CORONA Main Coronavirus thread

Zoner

Veteran Member
(fair use applies)


Why many more people are lining up for a flu shot than a Covid vaccine
Helen Branswell
By Helen Branswell Jan. 22, 2024

America is over the Covid vaccine.

Frantic lineups for scarce doses when Covid vaccines first became available have long since given way to widespread indifference. Each new round of boosters has drawn fewer bared arms than the round before it. The Centers for Disease Control and Prevention estimates that, as of Jan. 6, a mere 21.5% of Americans aged 18 and older and 11% of children have been vaccinated with the latest Covid vaccine.

But before you write off that number as a reflection of hesitancy over vaccines overall, consider this: 46.7% of Americans aged 18 and older and 47.5% of children have been vaccinated against influenza for this cold and flu season. In older adults, who are at the greatest risk from Covid, the gap is wider still; 73% of people 65 and older have received a flu shot, but only 41% have taken the Covid booster.

Why the disparity? Americans who regularly get a flu shot are just the type of people you’d expect would routinely get vaccinated against Covid. Yet as the statistics reveal, even many of them appear to have declined the latest booster.


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It’s not clear that a single definitive answer exists; in fact there is likely a combination of explanations, say people who study vaccine acceptance and vaccine hesitancy. They see this group as both a missed opportunity and as a cohort that could be swayed.

Jason Schwartz, an associate professor of health policy at the Yale School of Public Health, called people who get vaccinated against flu “the lowest hanging fruit for increasing Covid vaccine uptake.”

“These are people who are signaling right by their very actions that they are supportive of vaccines generally and that they’re supportive of the idea of an annual vaccination effort, even [with] a vaccine that is known to be less than perfect,” said Schwartz, who specializes in vaccine policy. “And the fact that those individuals are in some sense voting with their feet by … passing on Covid is a real warning sign above and beyond all the other issues these vaccination efforts face.”

The experts with whom STAT spoke about this issue expressed little surprise at the chasm between flu vaccine and Covid vaccine acceptance rates. While there are a striking number of similarities between the two vaccines — similarities health authorities might be advised to highlight more in their promotional efforts for Covid shots, some experts say — there are also intractable differences.

“I think it’s generally true that people who get flu shots are higher seekers of health care, and maybe put a greater premium on their health than people who don’t get flu shots. But … I think that the Covid vaccine is kind of in a different category,” said Sara Gorman, executive director of Those Nerdy Girls, a collective of women scientists and clinicians that formed — initially under the banner Dear Pandemic — to answer questions and dispel misinformation about Covid-19. (The group has since broadened its focus to encompass other scientific topics as well.)

For starters, there’s a veneer of politics clinging to the Covid vaccine that staid old flu vaccines do not have.

“Getting a Covid vaccine has come to symbolize identity politics in a way that no other vaccine really has,” said Gorman, who is the author of the upcoming book “The Anatomy of Deception: Conspiracy Theories, Distrust, and Public Health in America.”

“It is true that people on the left tend to get more vaccines in general. But even if you are sort of somewhere in the middle, and you still want your flu shot, but getting a Covid shot would mean associating yourself with a certain political identity that’s really not palatable to you, then you’re not going to do it,” she said.

Heidi Larson, director of the Vaccine Confidence Project, agreed, noting there is clear evidence of a political divide on Covid vaccine acceptance, with vaccination rates substantially higher among Democrats than among Republicans. Flu vaccine is simply not part of a political identity in that same way.

There is also a cloud of discomfort surrounding Covid vaccinations — questions about safety and effectiveness — that doesn’t hover over the flu vaccine, Schwartz noted.

He drew a parallel between the response to Covid vaccines and to HPV vaccines after the latter were first approved in the mid-aughts. Those vaccines prevent infection with human papillomaviruses that cause cervical, penile, and other cancers — viruses that are transmitted mainly by sex.

HPV vaccines are highly effective and work best when given before adolescents become sexually active. But vaccinating preteens and teens to protect them against a sexually transmitted infection is a bridge some parents have been reluctant to cross. Schwartz said it’s not unusual to see adolescents come in for medical appointments to get recommended vaccinations and leave having gotten a tetanus, diphtheria, and pertussis booster and a meningococcal vaccine but no HPV shot.

That kind of behavior is not uncommon when it comes to vaccines, Gorman said, with people agreeing to some but not others. “Most people are not in the camp of getting every single vaccine or not getting any vaccines,” she said.

Part of the unease with Covid vaccines relates to the unprecedented speed with which they were developed. Also at work, the experts said, are concerns about the messenger RNA platform used by the Pfizer and Moderna vaccines. These are the first approved vaccines that deploy mRNA to teach immune systems to protect against a threat. The vaccines have been given to hundreds of millions of people; there is overwhelming evidence they are effective and safe. But the mere notion of mRNA makes some people nervous.

“It’s a different technology, the mRNA technology, which people often don’t fully understand, and I think can be afraid of [it],” Gorman said.

Anti-vaccine campaigners have leaned into those fears, attempting to link Covid vaccines to a variety of serious side effects for which there is no scientific evidence. Larson pointed to the claims that erupt on social media when high-profile figures have sudden unexplained illnesses or young athletes die unexpectedly. “There have been some pretty awful social media campaigns like the whole sudden death thing. That really scares people,” said Larson, who is a professor of anthropology and risk at the London School of Hygiene and Tropical Medicine and the University of Washington at Seattle.

“Especially with Covid, that stuff really is in the air. And people do pick up on bits and pieces of it,” Gorman said.

The short-term side effects associated with the mRNA vaccines may also be contributing to reluctance. For some people, these vaccines are a breeze, but for others, a day or two of fever, aches, and chills are guaranteed to follow a booster. “We know from other vaccines that any mark in the ‘this is inconvenient for me’ column will suppress uptake,” said Malia Jones, an assistant professor of spatial dimensions of community health at the University of Wisconsin-Madison.

Legitimate scientific debate over how well boosters work and who needs additional shots at this point could also be fueling a sense of distrust among some individuals who are otherwise open to vaccination, the experts said. These debates aren’t happening about flu shots, which have been in routine use for decades. And it is clear some primary care providers are ambivalent about the need for additional Covid shots, and as a result may not be advocating strongly that their patients stay up to date. Study after study has shown that a firm recommendation from a trusted medical professional plays a huge role in persuading people to be vaccinated.

“I think in some cases, clinicians are not recommending them as strongly as they might for people who’ve already got … five, six, seven vaccines already,” said Jones, who personally knows some doctors who question whether another booster is necessary at this point.

These discussions, this ambivalence — they are not lost on people who are vacillating about whether to get a Covid shot, Schwartz said. “I think it can lead to both fatigue and confusion, saying, ‘Listen, even the experts can’t figure out sort of how to think about Covid vaccines. To hell with it.’”

He believes at this point the public undervalues Covid shots and underestimates the risk the illness presents.

“We continue to see studies showing the benefits of those additional doses in terms of the new responses and in terms of outcomes. And I think, increasingly, they seem to just sort of land with a thud. I don’t see them changing the public discourse,” Schwartz said.

Larson said people aren’t wrong to conclude that the risk from Covid has eased. Covid death rates are now, thankfully, a fraction of what they were two or three years ago. She believes the massive Omicron wave that began in late 2021 changed perceptions about Covid. The new variant was so adept at transmitting that massive numbers of people who had until then avoided Covid became infected in the early months of 2022. But the new version of the virus triggered less severe illness than the Delta variant that preceded it.

“That was like a turning point where people all of a sudden were like, ‘Oh, I think we’re out of the bad bit. It’s just like the flu, or a cold,’” Larson said. But flu isn’t benign, and furthermore, Covid is still more dangerous than flu, she noted.

In the first week of January, three-and-a-quarter times more people died from a Covid infection than from flu, according to CDC data. Drawing figures like those to the public’s attention might move some people who are on the fence, she said. “It’s not going to change the extremists’ minds.”

Larson thinks health authorities should play up the similarities between flu vaccination and Covid vaccination to appeal to more people who will take the former but not the latter. Like the fact that both vaccines have to be updated regularly because the viruses evolve. Like the fact that neither vaccine offers failsafe protection against infection, but both lower the risk of serious illness and death. Like the fact that with both flu viruses and SARS-2, immunity induced by vaccination or infection wanes, and therefore revaccination is required.

People understand these things about flu vaccine. These facts are baked into their acceptance of the need for an annual flu shot. But paradoxically, with Covid, these features seem to fuel distrust of the vaccines. People who catch flu after having a flu shot surmise they would have been sicker but for the vaccine. But if people see someone they know received a Covid booster go on to get infected, they conclude the shot isn’t worthwhile, Gorman said.

Flu vaccine has a clear advantage, thanks to the fact it’s been around for eons. People don’t really have to devote too much brain time to a decision. “It’s become normalized, become a routine,” Schwartz said.

Jones believes that that’s a big part of the problem in persuading people to get vaccinated against Covid. She has talked to parents about why their kids got a flu vaccine but not a Covid shot. “It’s just still too new,” she was told. And some of the questions people quite reasonably pose — Do we need annual shots? Does everyone need an annual shot? — can’t yet be answered. That adds to the discomfort, she said.

Jones thinks there will eventually be a standing recommendation from the CDC that everyone get a Covid shot every autumn, along the lines of the recommendations for the flu vaccine. “That would help signal to some of these folks who get an annual flu vaccine that this is on a schedule. It has to be updated every so often in order to keep our immunity fresh,” Jones said.

She and others said, however, that while there are ways to make inroads with the population of people who get annual flu shots, it’s going to take time. And even then, there will be people who will not be swayed.

“I don’t think there’s any magic fix for these things. But I do think sometimes those kinds of nudges help a bit,” said Larson. “But it’s only going to be for the people that are maybe leaning to yes but are not convinced enough.”
People don't realize that they have the mRNA in the flu shots as well.
 

amarah

Contributing Member
Thank you for the info! Bad news that Ivermectin is only good for the "earlier" strains of Covid and not the later ones. And, since the drug was made to fight intestinal parasites, it makes sense that taking it too long would mess up one's intestinal flora:

"Dysbiosis is when there is a problem with the diversity of someone’s gut bacteria. Though it is sometimes asymptomatic, dysbiosis may manifest in abdominal pain, bloating, and vomiting." Dysbiosis: Causes, treatments, and more

I hate to hear this, though. I had hoped the combo of ivermectin and hydroxychloroquine plus all the rest of the FLCCC protocol would continue to keep us safe.

But................viruses' prime characteristic........mutation.........
Could someone please point me to the article about IVM being good for only the earlier strains?I tried to go back and look but I can't find it.Thank you!
 
Yes. I have therapeutic teas from Thailand. I was in our local vitamin and supplement store yesterday and I noticed there are a lot of therapeutics out there dealing with Covid. I looked on the labels and they all had curcumin and turmeric in them.
I need to look into that as well.
 

Heliobas Disciple

TB Fanatic
(fair use applies)


Ottawa's use of Emergencies Act against convoy protests was unreasonable, violated Charter, court rules
Government says it plans to appeal the decision

Catharine Tunney · CBC News
Posted: Jan 23, 2024 12:49 PM EST | Last Updated: 12 hours ago

A federal judge says the Liberal government's use of the Emergencies Act in early 2022 to clear convoy protesters was unreasonable and infringed on protesters' Charter rights.

In what's already turning into a divisive decision, Federal Court Justice Richard Mosley wrote that while the protests "reflected an unacceptable breakdown of public order," the invocation of the Emergencies Act "does not bear the hallmarks of reasonableness – justification, transparency and intelligibility."

"I conclude that there was no national emergency justifying the invocation of the Emergencies Act and the decision to do so was therefore unreasonable and ultra vires," he wrote in a lengthy decision released Tuesday. "Ultra vires" is a Latin term used by courts to refer to actions beyond the scope of the law.

The Federal Court case was argued by two national groups, the Canadian Civil Liberties Association and the Canadian Constitution Foundation, and two people whose bank accounts were frozen. They argued Ottawa did not meet the legal threshold when it invoked the legislation, which had never been used before.

The federal government says it already plans to appeal.

Prime Minister Justin Trudeau's government invoked the Emergencies Act on Feb. 14, 2022 after thousands of protesters angry with the Liberals' response to the COVID-19 pandemic, including vaccine requirements, gridlocked downtown Ottawa for nearly a month and blocked border points elsewhere across the country. The protests gained international attention for bringing parts of the capital city to a halt.

The act gave law enforcement extraordinary powers to remove and arrest protesters and gave the government the power to freeze the finances of those connected to the protests. The temporary emergency powers also gave authorities the ability to commandeer tow trucks to remove protesters' vehicles from the streets of the capital.

Under the Emergencies Act, a national emergency only exists if the situation "cannot be effectively dealt with under any other law of Canada." Further, a public order emergency can be declared only in response to "an emergency that arises from threats to the security of Canada that are so serious as to be a national emergency."

The act defers to the Canadian Security Intelligence Service's definition of such threats — which includes serious violence against persons or property, espionage, foreign interference or an intent to overthrow the government by violence.

The government cited the situation in the Alberta border town of Coutts when it invoked the act. In the early hours of Feb. 14, before the act was invoked, Mounties in Coutts seized a cache of weapons, body armour and ammunition.

Four men are now awaiting trial, accused of conspiring to murder RCMP officers.


Economic orders infringed on Charter rights: judge


Mosley said the situation created by the protests across the country did not meet the CSIS threshold.

"The potential for serious violence, or being unable to say that there was no potential for serious violence was, of course, a valid reason for concern," he wrote. "But in my view, it did not satisfy the test required to invoke the Act, particularly as there was no evidence of a similar 'hardened cell' elsewhere in the country, only speculation, and the situation at Coutts had been resolved without violence."

Mosley's decision also examined one of the most controversial steps taken by the government in response to the protests — the freezing of participants' bank accounts.

"I agree with the [the government] that the objective was pressing and substantial and that there was a rational connection between freezing the accounts and the objective, to stop funding the blockades. However, the measures were not minimally impairing," he wrote.

The judge said the economic orders infringed on protesters' freedom of expression "as they were overbroad in their application to persons who wished to protest but were not engaged in activities likely to lead to a breach of the peace."

He also concluded the economic orders violated protesters' Charter rights "by permitting unreasonable search and seizure of the financial information of designated persons and the freezing of their bank and credit card accounts."

The two men whose bank accounts were frozen also argued that their rights under the Canadian Bill of Rights were violated, but Mosley disagreed.

He also concluded that the government's actions did not infringe on anyone's right to freedom of peaceful assembly.


Government plans to appeal

Noa Mendelsohn Aviv, executive director of the CCLA, said their win sets a clear and critical precedent for future governments.

"Emergency is not in the eye of the beholder. Emergency powers are necessary in extreme circumstances, but they are also dangerous to democracy," she said. "They should be used sparingly and carefully. They cannot be used even to address a massive and disruptive demonstration if that could have been dealt with through regular policing and laws."

Joanna Baron, executive director of the Canadian Constitution Foundation, said the decision is a "huge vindication for many people."

"[Mosley] also mentioned that economic disruption cannot form the basis for the invocation of extraordinary measures such as those contained in the Emergencies Act, which I think would lead to a very disturbing precedent across Canada, for example in the event of labour strikes and disruptions," she said.

The government has long argued the measures it took under the Emergencies Act were targeted, proportional and temporary.

Deputy Prime Minister Chrystia Freeland told reporters at a cabinet retreat in Montreal on Tuesday that the government plans to appeal the decision, setting up a legal battle that could go all the way to the Supreme Court of Canada.

"We believed we were doing something necessary and something legal at the time," she told reporters on Tuesday. "That continues to be my belief today."

"This was an extremely tense time. The safety of individual Canadians was under real threat … Our national security was under real threat – our national security, including our economic security," she said Tuesday.

Speaking alongside Freeland on Tuesday, Public Safety Minister Dominic LeBlanc said that the situation at Coutts and other border crossings helped to inform the government's decision to invoke the act.

"It's not banal when the security services tell you that they found two pipe bombs and 36,000 rounds of munition and ended up laying criminal charges as serious as to commit murder," he said. "So the context is important."

Mosley said those findings were "deeply troubling" but suggested the threats were being dealt with by the police of provincial and local jurisdiction outside Ottawa.

The judge wrote that it may be "unrealistic" to expect the federal government to wait when the country is "threatened by serious and dangerous situations," as the provinces or territories decide whether they have the capacity or authority to deal with the threat.

"However, that is what the Emergencies Act appears to require." he said.


Rouleau commission reached different conclusion

A mandatory inquiry, led by Commissioner Paul Rouleau, reviewed the government's use of the Emergencies Act in the fall of 2022 and came to a different conclusion.

After hearing from dozens of witnesses and reviewing thousands of never-before-seen documents, including cabinet ministers' text messages, Rouleau concluded the federal government met the "very high" threshold needed to invoke the Emergencies Act, citing "a failure in policing and federalism."

"Lawful protest descended into lawlessness, culminating in a national emergency," he wrote.

Justice Minister Arif Virani said the government cited Rouleau's conclusions when discussing the government's decision to appeal Mosley's ruling.

"[Rouleau's] decision stands at odds with the decision that was rendered today and I think that is important and that also informs our decision to appeal," Virani told reporters Tuesday.

CSIS Director David Vigneault testified that he supported invoking the Emergencies Act, even if he didn't believe the self-styled Freedom Convoy met his agency's definition of a threat to national security.

In his final report, Rouleau argued that the definition of "threats to the security of Canada" in the CSIS Act should be removed from the Emergencies Act.

Rouleau, an Ontario Court of Appeal justice, said he reached his conclusion with some reluctance.

"I do not come to this conclusion easily, as I do not consider the factual basis for it to be overwhelming," he said in statements he gave after his report was made public.

"Reasonable and informed people could reach a different conclusion than the one I have arrived at."

Mosley heard arguments in court over three days last April. He wrote that at the outset of the proceedings, he felt the protests in Ottawa and elsewhere went "beyond legitimate protest and reflected an unacceptable breakdown of public order."

He said he reached his decision "with the benefit of hindsight" and a more extensive record of facts and law than cabinet had available to it when it made its decision.


Political reaction


Conservative Leader Pierre Poilievre was quick to condemn the government and Prime Minister Trudeau personally.

"He caused the crisis by dividing people," he posted on the social media platform X. "Then he violated Charter rights to illegally suppress citizens. As PM, I will unite our country for freedom."

NDP Leader Jagmeet Singh said that his party reluctantly supported the invocation of the act.

"The reason we were in that crisis was a direct failure of Justin Trudeau's leadership and also other levels of government that failed to act," he said during a caucus meeting in Edmonton.

Singh said his party will watch to see where the appeal goes.
 

Heliobas Disciple

TB Fanatic
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COVID variant JN.1 is not more severe, early CDC data suggests
Alexander Tin - CBS News
Updated Tue, January 23, 2024, 10:14 PM EST

Early data from hospitals suggests the latest COVID variant, known as JN.1, is not leading to more severe disease, a Centers for Disease Control and Prevention official said Monday, as the agency has tracked the strain's steep rise to an estimated 85.7% of COVID-19 cases nationwide.

The agency is still waiting for more weeks of data to lay out its more detailed assessment of JN.1's impact this season, the CDC official, Dr. Eduardo Azziz-Baumgartner, said at a webinar with testing laboratories hosted by the agency this week.

Asked if JN.1's symptoms seemed to be more severe compared to previous waves, he said "there are early signals that that may not be the case," based on electronic medical record cohorts and other data.

"Now, it's important to remember that how a virus affects an individual is a unique 'n' of one," he added. "It could be very severe. People could die from a virus that, to the general population, may be milder."

Azziz-Baumgartner told the webinar the CDC hopes to release more details about JN.1's severity "during the next couple weeks" as more data on the virus accumulates.

So far, the CDC has been careful to say that there was "no evidence" JN.1 was causing more severe disease, even as it contributed to the spread of the virus this winter.

It is not clear when the CDC's new assessment of JN.1 is scheduled to be published. A CDC spokesperson was not able to immediately respond to a request for comment.

Scientists at the CDC and other federal health agencies have also so far not moved to deem JN.1 a standalone "variant of interest," in a break from the WHO's decision to step up its classification of the lineage last month.

The WHO said Friday that there were "currently no reported laboratory or epidemiological reports" linking JN.1 or its other variants of interest to increased disease severity.

CDC's early findings about JN.1 come as the agency has begun to see a slowing of respiratory virus trends after a peak over the winter holidays.

The agency's disease forecasters also concluded earlier this month that JN.1's spread did not warrant them stepping up their assessment of COVID-19's threat this winter, noting hospitalization rates appeared to be lower than they were last season.

COVID-19 hospitalizations this season continued to outpace influenza nationwide, the agency's data suggests, and weekly rates of both stopped short of topping previous record highs.

Azziz-Baumgartner cautioned data lags could be muddying the picture, as hospitals catch up on delayed reporting of their weekly admissions. Officials have also been closely watching for possible signs of a renewed increase in the spread of influenza, as has been seen in some previous seasons before the COVID-19 pandemic.

Some jurisdictions have also been reporting a strain on hospitals, especially in New England, he said. CDC figures tally the region's hospital capacity rate as the worst in the country.

Massachusetts General Hospital warned last week it was taking steps to address an "unprecedented overcrowding" crisis, along with other hospitals in the state.
 

Heliobas Disciple

TB Fanatic
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IgG4 against Nucleocapsid is no excuse: There is zero evidence of a class shift after infection
Radagast
January 22, 2024

So a few days ago I pointed out that all the excuses for the IgG4 antibody class shift after vaccination don’t hold up. We don’t see it happening in any unvaccinated people and we don’t see it happening after non-mRNA vaccination either. It’s a problem uniquely associated with the mRNA vaccines, which have been administered to more than 90% of the adult population in some countries.

I will have to address some more bullshit by the vaccine peddlers. I already know two or three people will read this post at most, but people asked me about this, so I will give them what they ask.

The idea being proposed by some is that IgG4 is together with IgG2 part of some normal compensatory response that inevitably has to happen after sufficient exposure to SARS-COV-2. But that’s not true. All the data we have suggests that there is no transition to IgG4 after infection. It’s not a normal compensatory biological mechanism.

The reason the IgG4 antibody class shift happened is because you gave people a “vaccine” that misrepresented what was going on to the immune system. The Spike protein was displayed on the surface of otherwise healthy cells in the absence of pro-inflammatory signaling, because these cells had been fooled into expressing this protein. When you do this often enough, you train the immune system to tolerate the Spike protein. It starts to think of those parts of the Spike protein that you want the antibodies to neutralize, as normal human proteins that need to be tolerated.

So the argument you often see peddled, is that this is not a problem, but part of a normal compensatory response, because there exist IgG4 antibodies against Nucleocapsid. But that’s not a valid argument and I will explain why. One of my commenters asked:
Now she sent me this study: Seroprevalence of IgG and Subclasses against the Nucleocapsid of SARS-CoV-2 in Health Workers ( Seroprevalence of IgG and Subclasses against the Nucleocapsid of SARS-CoV-2 in Health Workers ) and I would be terribly grateful how to interpret this as they do show elevated IGg4 level in unvaccinated health workers against nucleocapsid protein and how that differs from Spike protein and how that applies (or it doesn’t) to latest IGg4 studies.
The answer is basically as following:

Your body produces IgG4 and IgG2 against stuff it needs to tolerate. Viruses typically evolve in a way that makes their proteins look similar to your own proteins, so that you can’t deploy an aggressive antibody response to those proteins without damaging your own body. For SARS-COV-2, the Nucleocapsid protein looks very similar to the Nucleocapsid protein in other corona viruses that regularly infect us. The Nucleocapsid protein has regions that look very similar to some of our own proteins, so you will find some IgG4 against certain regions when people are exposed to the virus.

However, this doesn’t matter much, because the Nucleocapsid protein is not the protein your body can use to neutralize the virus anyway, such antibodies can only help recognize infected cells and clean up viral debris. There’s a reason they vaccinated against Spike: It’s the only protein your can use to get antibodies that will neutralize the virus. Antibodies against the other proteins can not stop a viral particle from entering a cell.

In addition, we don’t see evidence of what these people are proposing, that the immune response shifts to IgG2 and IgG4 in response to sufficient exposure to the virus. This is not seen for antibodies against Spike, nor is it seen for antibodies against the Nucleocapsid protein. There are parts of the Nucleocapsid protein your body needs to tolerate, because they resemble your own proteins. Those antibodies may increase in concentration, but we see no evidence of a class shift to IgG2 and IgG4 against Nucleocapsid after SARS2 infection.

In simple English:

The immune system does not respond to SARS2 infection by learning to tolerate bits protein that it used to aggressively fight.

It keeps tolerating stuff that it already tolerated, sure. If the virus has sequences it tolerates, antibody concentrations against those sequences will rise, sure.

But what you don’t see, is the immune system moving from aggressively fighting certain sequences, to tolerating those sequences from now on. We have no evidence that this occurs in people, not even after severe infections from this virus.

That only appears to happen when you give people a bad vaccine, that makes the Spike protein look like just another normal protein that some of your own cells naturally happen to express.

———————

The evidence

They find that in healthcare workers, the detected subclasses were: IgG1 (82.4%), IgG2 (75.9%), IgG3 (42.6%), and IgG4 (72.6%). Why would IgG3 only show up in 42.6% of the healthcare workers? Because these workers were being studied outside of the context of any recent infection. IgG3 antibodies normally decline rapidly in most people. When you try to keep their levels high with regular booster shots, to protect people from reinfection, you start breaking stuff.

To understand these results and to find out if there is some sort of natural shift towards anti-inflammatory IgG2 and IgG4 antibodies, we can look at this study:

Serological analysis reveals an imbalanced IgG subclass composition associated with COVID-19 disease severity

I’m going to quote the results for you here.



So yes, you see 9% antibody prevalence against Nucleocapsid. But you see just 1% with any detectable IgG4 antibodies against the Spike protein.

So is there evidence of some sort of class shift towards IgG2 and/or IgG4 in a severe infection? That’s the sort of situation where you would expect such a class shift to happen, if this is a real thing. So do we see evidence of it?

No. Not for Spike protein. And not for Nucleocapsid protein either. Look with me at this:



You can look for yourself here. There’s no evidence of a class shift towards IgG4. IgG4 and IgG2 increase in concentration as the infection becomes more severe, sure.

But look at IgG1 and IgG3, the normal antibodies you want to see. Their concentrations grow much more relatively than IgG2 and IgG4, for every protein! What you see is the opposite of a class shift: As the infection gets more severe, the body sends more and more IgG1 and IgG3 after those parts of the virus that look unlike any of your own proteins.

So why is there IgG4 detected against Nucleocapsid at all?

Easy.

First of all, a lot of Nucleocapsid consists of sequences you find in all the hCOvs, as well as commensal bacteria:

COVID-19 patients elicit strong responses to the nucleocapsid (N) protein of SARS-CoV-2 but binding antibodies are also detected in prepandemic individuals, indicating potential crossreactivity with common cold human coronaviruses (HCoV) and questioning its utility in seroprevalence studies.
So when a part of the Nucleocapsid looks like something found in your gut bacteria, you will develop IgG2 antibodies against that part and perhaps IgG4. If you’re then infected by the virus, those concentrations will go up.

Second, parts of the Nucleocapsid looks like some of your own proteins, so of course your immune system can’t send aggressive pro-inflammatory antibodies after those parts:
We hypothesized that immunodominant epitopes of SARS-CoV-2 share homology with proteins associated with multiple sclerosis (MS). Using PEPMatch, a newly developed bioinformatics package which predicts peptide similarity within specific amino acid mismatching parameters consistent with published MHC binding capacity, we discovered that nucleocapsid protein shares significant overlap with 22 MS-associated proteins, including myelin proteolipid protein (PLP). Further computational evaluation demonstrated that this overlap may have critical implications for T cell responses in MS patients and is likely unique to SARS-CoV-2 among the major human coronaviruses.
You can expect your immune system to deploy IgG4 antibodies against these sequences. That’s normal, it helps prevent you from attacking your own healthy cells.

But when the immune response against SPIKE is dominated by IgG2 and IgG4? That’s a problem. It’s the only protein we know of, that allows your antibodies to neutralize viral particles.

Your own immune system never does that, not even after severe infections by this virus. Look at IgG4 against all the proteins in mild, vs moderate vs severe cases, in the graph I posted above. You don’t see the body switching to IgG4, against any of the proteins.

So sorry, the fact that you can find some IgG4 against nucleocapsid doesn’t bail us out. It’s not evidence that a tolerogenic class shift against Spike is a normal response to the virus.

Again, you’re still stuck with the worst case scenario.

You broke the antibody response, there are now amino acid sequences found in the Spike protein that more than a billion people worldwide were taught to tolerate. Every other pathogen now has a massive incentive to mutate, to incorporate those sequences people’s immune systems were taught to tolerate.

The other vaccines have failed too, they made the long term outcome of this pandemic much worse, by fixating people’s response on an extinct version of the virus. But there’s nothing quite as insane, as the failure of the mRNA vaccines.
 

Heliobas Disciple

TB Fanatic
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COVID-19 Hospitalizations Up By 12.8 Percent In Thailand While Worrisome JN.1 Spawns JN.1.4, JN.1.1.3, JN.1.6 Debuts In The Country

James Rosh - Thailand COVID-19 News
Jan 23, 2024

Latest reports from Thailand’s Department of Disease Control (DDC) shows that COVID-19 hospitalizations have by about 12.8 percent in the past week when compared to the preceding week.

The latest figures from Thailand’s DDC though lacking total number of daily COVID-19 testing undertaken or even the COVID-19 test possivity rates and are likely to be well below the actual figures, still reflect a worrisome scenario.


A total of 718 individuals were admitted to hospitals due to COVID-19 disease severity during the period 14th of January 2024 to 20th January 2024.(note that certain private hospitals in the country are insisting that the actual figures could be far much more as they are already overwhelmed at their own hospitals.

According to the DDC, average daily admissions had increased to about 102 from 89 during the previous 7 days between 7th-13th of January 2024.

The total number of deaths for the latest epidemiological week also sadly showed an increase of deaths with 11 individuals reported dead due to COVID-19. (We do however advise readers to carefully study the excess death rates in Thailand to get a realistic perspective of the actual deaths that COVID-19 is driving in the country!) It was reported that of the dead, almost all were elderly individual and some with most having existing comorbidities. 5 had completed the two dose COVID-19 vaccine regimens while the remining 6 were unvaccinated.

Of the 718 new hospital admissions, 209 were reported to be having serious ARDs conditions with their lungs severely compromised.

A total of 149 are on ventilators of which 142 were fully vaccinated individuals who had received boosters while only 42 were unvaccinated.

This shocking revelation questions the efficacy of the vaccines and boosters in protecting against disease severity.

Already a lot of Thai doctors and Thai healthcare professionals are raising concerns about the efficacy of the COVID-19 vaccines and also about the adverse effects that it is causing.


A recent Thai study has also showed homologous doses of the Pfizer RNA vaccines increases the risk of myocarditis and pericarditis.


While ignorant doctors and also many dumb ‘journalist’ from local Thailand COVID-19 News outlets and even garbage news aggregator sites or forums run by British boiler room scammers, Australian pedophiles and Russian criminals are claiming that the JN.1 variant are behind the current surge, there are actually many other SARS-CoV-2 strains and sub-lineages still in circulation in Thailand and are also playing a key role behind the current surge which has been and will be a long wave in the sense the surge will be over a long period of time and it not the least expected to reach a peak or end anytime soon.


The fact of the matter is that there are many other JN.1 spawns with unique mutations and even possibly different pathogenic behaviors now at play globally and even in Thailand and that even the JN.1 variant should not be much of concern compared to these newer spawns.

Data from GISAID and also from the CoV-Spectrum platform shows that a number new JN.1 sub-lineages such as JN.1.1, JN.1.1.1, Jn.1.4, JN.1.1.3 and JN.1.6 have already made their debut in Thailand.


(look at lineages)

Of these, the below JN.1 spawns or sub-lineages that have made their recent debut in Thailand and could possibly be the ones driving disease severity. However, detailed studies are needed to validate this.

JN.1.1 (9 sequences so far)


JN.1.4 (sequences so far)


JN.1.1.3 (2 sequences so far)


JN.1.1.1 (1 sequence so far)


JN.1.6 (1 sequence so far)


Note that most of these sequences were from samples taken from hospitalized individuals exhibiting disease severity and ARDs.

Thailand should also be wary of the even more concerning strains like JN.1.11, JN.1.2 and JN.1.6.1 reaching the country.


https://www.thailandmedical.news/ne...bout-is-now-increasing-in-spread-across-india

Thai Health authorities at the moment insist that the JN.1 strain is not exhibiting any signs that it drives disease severity.

Meanwhile, health authorities in Thailand are saying that they are seeing many in the current COVID-19 surge developing symptoms like coughing, muscle pain, sore throat, headache, and a runny nose.

The Thai Disease Control Department is advising locals and expats in the country to not to let their guard down and to take precautions by wearing face masks whenever they are in crowded places, such as on public transport or in hospitals, to wash their hands frequently and to take a COVID-19 ATK test if they develop flu-like symptoms.
 

Heliobas Disciple

TB Fanatic
(fair use applies)


18,677 Japanese Hospitalized For COVID-19 As Of 17th January 2024 Yet No Media Covering The Unfolding Crisis
Nikhil Prasad Fact checked by:Thailand Medical News Team
Jan 23, 2024

Affected citizens in Japan are reporting that in certain prefectures and even in Tokyo itself, access to doctors or a healthcare facility to see treatments for respiratory infections and even COVID-19 is difficult as not only are queues long for outpatient clinics but ERs are overwhelmed and hospitals beds are becoming scarce.

Pharmacies and drug stores are not only out of COVID-19 ATK test kits but stocks of “cold medicines” such as cough syrups, NSAIDS and even nasal decongestants are simply running out especially those for pediatric use.

Data from Sapporo medical University that was last updated on the 14th of January 2024 shows alarming rise of COVID-19 across almost all prefectures across Japan with Aichi, Hokkaido and Tokyo the most affected areas.


Data release by the Japanese Ministry of Health, Labour and Welfare as of the January 19th 2024 shows COVID-19 Infections and hospitalizations rising at a rapid and worrisome phase. In the second week of January 2024, Japan saw more than 44,000 new COVID-19 infections nationwide.


新型コロナウイルス感染症に関する報道発表資料(発生状況等)2023年6月~

療養状況等及び入院患者受入病床数等に関する調査について

As of the 17th of January 2024, there were 18,677 Japanese individuals hospitalized due to COVID-19.


Interestingly, no local Japanese COVID-19 News media or international wire agencies are covering about the unfolding crisis in Japan possibly due to discreet censorship imposed by certain politicians.

Also we have not been able to procure accurate data on COVID-19 deaths and excess mortality figures In Japan for the last 4 weeks and hence are not able to make any comments despite being fed depressing speculatives by doctors we have spoken to in the last few hours.

While the JN.1 variant is currently the predominant variant in Japan accounting for almost 59 % of all genomic sequences, newer JN.1 spawns have also emerged in the country such as JN.1.1, JN.1.4, JN.1.5, JN.1.7. JN.1.8 JN.1.9 and worryingly the JN.1.2 sub-lineage.


https://www.thailandmedical.news/ne...nks-likely-to-be-the-next-predominant-variant

Thailand Medical News will be providing more updates on the situation in Japan within the next 24 hours as we have contacted some local stringers to assists up with more data and personal interviews.
 

psychgirl

Has No Life - Lives on TB
I notice mention of long term use of IVM being the problem, like antibiotics do. That’s why I won’t use it until I actually need it. I think high intracellular zinc and vitamin D3 are simpler and far harder to evolve around than more complex treatments, and are better used as prophylactics.
You “could” be right.
We are still using it 1-2 weekly as a prophylactic.
Maybe this spring/summer I’ll discontinue for awhile. Will see.
 

Heliobas Disciple

TB Fanatic
(fair use applies)


While Official Data Claims COVID-19 Cases Decreasing Nationwide, Hospitals In Massachusetts On Verge Of Collapsing
Nikhil Prasad Fact checked by:Thailand Medical News Team
Jan 24, 2024

Data from the U.S. CDC and from the new firm that the U.S. government has contracted for waste water surveillance i.e Verify…a company that belongs to Google!...claims that COVID-19 cases are declining nationwide, data from individual states and counties are showing the opposite.

In the state of Massachusetts, data shows that COVID-19 infections and hospital admissions were still high. From data released by the Massachusetts Department of Health, for the week 7th of January 2024 to 13th January 2024, there were a total of 41 COVID-19 deaths and there were 5491 COVID-19 cases.


However, for Emergency Department visits for various respiratory infections, a total of 63,323 visits were recorded for the same week.


It should be noted that the manner of reporting COVID-19 data by the Massachusetts government is devised to try to mislead anyone into understanding the actual COVID-19 scenario. They do not publish number of COVID-19 test conducted, the test posivity rates and actual COVID-19 hospital admissions.

However, latest COVID-19 News - United States updates are showing that various hospitals across the state are not only overwhelmed but also on the verge of collapsing.

Mass. General declares 'capacity disaster'


Massachusetts General Declares Code Help

Massachusetts General Hospital. One of the largest hospitals in the states has declared a "capacity disaster" as it grapples with an unprecedented crisis, requiring a significant increase in hospital beds to address a surplus of patients.

The situation, characterized by the hospital as a full-blown crisis, has persisted for the past 16 months, with the Emergency Department (ED) consistently operating at critical capacity levels. Patients are experiencing extended wait times for inpatient beds, with the ED frequently placed in a state of "Code Help" or "Capacity Disaster."

The crisis is exacerbated by the surge in illnesses such as COVID-19, flu, RSV, and other winter viruses. In a statement, a hospital spokesperson explained that "Code Help" occurs when inpatient beds and hallway stretchers are full, while "Capacity Disaster" is triggered when the ED reaches full capacity, all hallway stretchers are in use, and there are over 45 inpatients waiting for a hospital bed. Between October 2022 and September 2023, patients spent a total of 381,228 hours boarded in the hospital's ED, reflecting a 32 percent increase from the previous 12-month period.

In September alone, Mass. General saw patients boarding for a median of 14.1 hours, and 26 percent of admitted patients remained in the ED for more than 24 hours. Hospital President David F.M. Brown characterized the situation as a full-blown crisis for both emergency patients and healthcare workers, attributing it to the heightened demand for care in the post-pandemic era. Brown emphasized that 50 to 80 patients spend their first night of hospitalization in the ED daily, an inappropriate and non-therapeutic environment that significantly contributes to clinician burnout and frustration.

However, in the last three weeks, COVID-19 cases have exacerbated the situation to a point that the hospital directors are warning that the hospital services might simply collapse


View: https://twitter.com/MassGeneralNews/status/1748409540712812863


Mass. General is not alone in facing this challenge, as numerous hospitals in Massachusetts struggle with patient overflow. In response, hospitals statewide are prioritizing faster discharges to free up beds. Some health insurance providers have also agreed to waive prior authorizations that may delay patient discharge. The hospital has provided information on its response to the crisis on a dedicated webpage, urging the public to stay informed about the ongoing situation.

Other hospitals in Masschusetts like Beth Israel Deaconess Medical Center, Tufts Medical Center, Lahey Hospital and Medical Center and UMass Memorial Medical Center are all reporting almost similar situations with their ER departments being overwhelmed in the last 4 weeks and a shortage of COVID-19 beds.

The Massachusetts government has not made an official public announcement about the COVID-19 situation in the state or about what they are doing to deal with the situation.

Thailand Medical News will be providing more updates on the COVID-19 situation in Massachusetts.
 

Heliobas Disciple

TB Fanatic
(fair use applies)


SARS-CoV-2 Develops Mutations That Causes Resistance To Any Antivirals Used. In Japan, Use Of Ensitrelvir Resulted In M49L Mutants
Nikhil Prasad Fact checked by:Thailand Medical News Team
Jan 24, 2024

Since the onset of the SARS-CoV-2 pandemic in 2020, the quest for effective antiviral therapies has been a focal point of medical research. As witnessed in previous viral outbreaks, such as Influenza and HIV, the development of potent antiviral treatments plays a pivotal role in managing public health crises. Initial hopes were pinned on the repurposing of broad-spectrum antivirals targeting the replication complex. However, clinical trials yielded disappointing results, leading researchers to explore alternative avenues as reported in various past COVID-19 News coverages.

Nirmatrelvir (Paxlovid®), a 3CLpro inhibitor, emerged as a promising candidate, demonstrating robustness against variants in clinical trials according to claims by the pharma giant involved i.e. the notorious Pfizer. Another contender, ensitrelvir (Xocova®), developed by the Japanese company Shionogi, claimed encouraging results in Phase 2 trials and gained emergency regulatory approval in Japan in November 2022. However, recent developments raise concerns about the efficacy of these protease inhibitors, as experimental evidence suggests the emergence of resistance mutations.

Evidence is emerging that the SARS-CoV-2 virus ultimately develops mutations to confer drug resistance to any antivirals used. In the case of Paxlovid, the mutations T21I, T304I, L50F and E166A emerged.

Thailand Medical News had been warning about SARS-CoV-2 drug resistance since the time Remdesivir was being used.

https://www.thailandmedical.news/ne...se-inhibitors-multi-drug-approach-recommended

https://www.thailandmedical.news/ne...ral-paxlovid-many-such-variants-in-america-no

https://www.thailandmedical.news/ne...-is-responsible-for-antiviral-drug-resistance


https://www.thailandmedical.news/ne...atrelvir-a-component-of-paxlovid-mpro-binding


Experimental Generation of Resistant Strains

Researchers at the Unité des Virus Émergents, UVE: Aix Marseille Univ-France, in collaboration with the Drugs for Neglected Diseases Initiative in Geneva-Switzerland, conducted experiments to generate SARS-CoV-2 strains resistant to nirmatrelvir and ensitrelvir. Through 16 passages in vitro, they successfully produced mutants displaying resistance to these clinical stage protease inhibitors.

Notably, the M49L mutation was identified as a key player, conferring a robust resistance to ensitrelvir. In vitro analyses demonstrated a substantial loss of sensitivity for the resistance mutants, indicating a potential challenge in the effectiveness of these antivirals.


In Vivo Implications of the M49L Mutation

Utilizing a Syrian golden hamster infection model, the researchers observed that the ensitrelvir-resistant M49L mutation rendered ensitrelvir treatment ineffective in vivo. The study revealed that the M49L mutation alone significantly reduced the efficacy of ensitrelvir in the hamster model.

Furthermore, a noteworthy finding was the identification of an increasing prevalence of naturally occurring M49L-carrying sequences over recent months. This trend raised concerns about potential links between the rise in M49L mutants and the utilization of ensitrelvir in Japan since its approval in November 2022.


Genetic Monitoring for Treatment Efficacy

The experimental findings underscore the strategic importance of genetic monitoring of circulating SARS-CoV-2 strains to ensure the continued effectiveness of antiviral treatments. Resistance mutations, such as M49L, pose a substantial limitation to the efficacy of antiviral monotherapies. The study suggests that the emergence of these mutations may occur both naturally and in response to treatment conditions.

Nirmatrelvir (Paxlovid) and ensitrelvir (Xocova) demonstrated a certain degree of cross-resistance in vitro, implying that substituting one compound with the other could potentially mitigate the emergence of resistance during treatment. However, the magnitude of resistance observed with the M49L mutation in ensitrelvir raised concerns about the efficacy of this approach.


Global Prevalence of M49L-Carrying Sequences

The researchers conducted a comprehensive analysis of the global prevalence of M49L-carrying sequences through data obtained from the Global Initiative on Sharing All Influenza Data (GISAID). The study revealed that, as of October 30, 2023, a small proportion (0.00165%) of SARS-CoV-2 sequences carried the M49L mutation.

Notably, the prevalence of M49L has shown a recent increase, with more occurrences reported between May and October 2023 compared to the previous 21 months. The analysis identified Japan as the primary origin of M49L sequences, constituting 59.9% of the total sequences and rising to 88.3% in the specified time frame.


Association Between M49L Prevalence and Ensitrelvir Use in Japan

The study established a correlation between the increased prevalence of M49L and the introduction of ensitrelvir (Xocova) in Japan. The drug received emergency regulatory approval in November 2022 and was commercially available from April 2023. The researchers observed that the surge in M49L-carrying sequences coincided with the timeline of ensitrelvir use in the country.

Further analysis indicated that M49L sequences were sporadically observed before December 2022, with a significant upswing since June 2023. This temporal alignment strongly suggested a potential link between the selective pressure exerted by ensitrelvir use and the increased prevalence of M49L mutants.


Multiple Lineages and Emergence Events


To delve deeper into the genomic diversity of M49L-carrying sequences, the researchers examined the Pango lineage distribution. Surprisingly, M49L was found in 90 different lineages, including prominent ones like Alpha, Delta, and Omicron. This extensive distribution suggested that M49L had emerged independently on multiple occasions.

Phylogenetic analysis revealed 12 distinct emergence events associated with the M49L mutation, further emphasizing the repeated occurrence of this resistance-conferring mutation within the SARS-CoV-2 genome. This finding highlighted the importance of monitoring these emergence events to assess the risk of fixation of the mutation.


Implications for Antiviral Therapies


The study's findings have significant implications for the ongoing efforts to combat SARS-CoV-2. The emergence of resistance mutations, particularly the M49L mutation, raises concerns about the long-term efficacy of ensitrelvir. The observed increase in prevalence linked to ensitrelvir use in Japan underscores the need for vigilant genetic monitoring to adapt treatment strategies and prevent the spread of resistant strains.

The study advocates for continuous assessment of the risk associated with antiviral treatments, emphasizing the importance of a diversified arsenal of antivirals targeting various viral proteins. Additionally, the identification of resistance mutations like M49L necessitates a nuanced approach in treatment strategies, potentially considering dual therapies to mitigate the risk of resistance emergence.


Conclusion

In conclusion, the experimental generation of SARS-CoV-2 mutants resistant to nirmatrelvir and ensitrelvir, particularly the ensitrelvir-resistant M49L mutation, raises critical questions about the sustainability of current antiviral therapies. The study's comprehensive analysis of global prevalence and emergence events provides valuable insights into the dynamics of resistance mutations.

The correlation between ensitrelvir use in Japan and the surge in M49L prevalence highlights the intricate interplay between drug utilization and the evolution of viral strains. This study underscores the urgency of implementing genetic monitoring strategies to adapt antiviral treatments and mitigate the risk of resistance emergence.

As the world continues to grapple with the evolving landscape of the SARS-CoV-2 pandemic, ongoing research and surveillance are imperative to stay ahead of emerging challenges and to ensure the effectiveness of antiviral interventions in the face of a dynamic virus.

The study findings were published in the peer reviewed journal: Antiviral Research.

 

Heliobas Disciple

TB Fanatic
(fair use applies)


Florida Study Shows That Low-Dose Naltrexone Can Improve Long-COVID Symptoms
Nikhil Prasad Fact checked by:Thailand Medical News Team
Jan 24, 2024

Post–COVID-19 condition (PCC) has emerged as a complex and debilitating disease, characterized by persistent symptoms following the initial COVID-19 infection. The medical community has been actively exploring interventions to alleviate the symptoms of PCC, with limited success in randomized clinical trials (RCTs). This COVID-19 News report delves into a groundbreaking study conducted by the Veterans Affairs Medical Center in Miami, Florida, in collaboration with the University of Miami and Nova Southeastern University. The study investigates the efficacy of treatments adapted from myalgic encephalomyelitis and chronic fatigue syndrome (ME/CFS) for managing PCC symptoms. In particular, the study found that low-dose naltrexone can improve Long-COVID symptoms.

Thailand Medical News had also previously covered another American study that also showed similar results in that low dose naltrexone could help with the treatment of post-acute sequelae of COVID-19.

https://www.thailandmedical.news/ne...treatment-for-post-acute-sequelae-of-covid-19

The Florida Study Setting

The Miami Veterans Affairs Healthcare System's (VAHS) post–COVID-19 clinic, established in 2021, serves as a multidisciplinary center providing hybrid services, both remote and in-person. The clinic, comprising internal medicine providers, physical medicine and rehabilitation specialists, and nurse practitioners, plays a crucial role in addressing the unique challenges posed by PCC. Patients are referred by primary care providers or screened through a national VAHS digital prescreening pilot.

Baseline Characteristics

The study included 108 patients with PCC who initiated treatments, ensuring a minimum of 2 follow-up visits. The patients were categorized based on the treatments received, with the largest group receiving amitriptyline. Interestingly, those receiving a combination of amitriptyline and low-dose naltrexone were observed to be younger and with fewer comorbidities compared to those on duloxetine or undergoing physical therapy. These baseline characteristics set the stage for a comprehensive analysis of the effectiveness of different treatments.

Exploring Treatment Effectiveness

Drawing parallels between ME/CFS and PCC, the researchers adapted treatments proven effective in ME/CFS to the PCC population. Amitriptyline, duloxetine, and low-dose naltrexone, known for their efficacy in managing symptoms and inflammatory reactions in ME/CFS, were investigated. The study's findings revealed that low-dose naltrexone demonstrated superiority over physical therapy, while amitriptyline showed similar effectiveness. Furthermore, a noteworthy observation was the synergistic effect of physical therapy when combined with medications, suggesting a potential avenue for comprehensive treatment strategies.

The study sheds light on the effectiveness of low-dose naltrexone, amitriptyline, duloxetine, and physical therapy in managing PCC symptoms among veterans. The distinct impacts of these therapies on common symptoms underscore the importance of personalized and tailored treatment approaches. The findings not only contribute to the evolving understanding of PCC but also highlight the potential of repurposing medications previously used for similar symptoms in ME/CFS.

Conclusions

In conclusion, this Florida-based study provides crucial insights into the potential efficacy of medications, such as low-dose naltrexone and amitriptyline, for managing PCC symptoms. The observed differences in treatment impacts emphasize the need for personalized therapeutic strategies based on patient priorities. While the study offers promising results, the authors stress the necessity for formal RCTs to ascertain optimal dosages, target phenotypes, adverse events, and potential drug interactions. Future research endeavors should prioritize unraveling the underlying mechanisms of these medications, paving the way for more targeted and effective treatments for PCC. As the medical community continues to grapple with the challenges of PCC, studies like these provide hope and direction for improved patient outcomes.

The study findings were published in the peer reviewed journal: Clinical Therapeutics.

 

Heliobas Disciple

TB Fanatic
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mRNA Vaccines Contain Prion Region, May Be Linked to Prion-Like Diseases
As pathogenic prions accumulate, people may start to develop prion diseases such as Creutzfeldt-Jakob disease and mad cow disease.

By Marina Zhang
1/24/2024

The COVID-19 virus and its vaccine sequences have a prion region on their surface spike proteins. Earlier in the pandemic and vaccine rollout, some researchers were concerned that these prion regions may promote incurable prion diseases, such as Creutzfeldt-Jakob disease (CJD).

In December 2023, researchers from Oxford showed that 8 percent of the time, the body does not make spike protein from Pfizer mRNA vaccines but may form aberrant proteins instead. This has led researchers to investigate the potential risks of such unintentional formations.

Subsequently, on Jan. 12, retired French biomathematician Jean-Claude Perez published a preprint study discussing whether such mistakes could lead to the formation of prion-like proteins. He concluded that prion-like protein formation is possible
.
A previous peer-reviewed paper by Mr. Perez and his co-authors in January 2023 recorded 26 cases of CJD. Those afflicted reported that their first symptoms manifested within one to 31 days of their last COVID-19 vaccination or infection.

All patients experienced a rapid worsening of their condition over the ensuing months and died.


What Are Prions?

Prions are proteins that exist naturally in the brain. They perform crucial tasks and are necessary for human health.

However, on rare occasions, a healthy prion may misfold into a pathogenic prion. This misfold is irreversible, and from then on, the pathogenic prion converts all healthy prions it encounters into pathogenic prions.

As pathogenic prions accumulate, people may start to develop prion diseases such as CJD and mad cow disease.

Other researchers have also proposed that Parkinson’s disease and Alzheimer’s disease, both of which exhibit an accumulation of misfolded proteins, may also be prion diseases.

Prions are defined by their amino acid sequences. Prion-like sequences are rich in glutamine and asparagine amino acids, and human or foreign proteins that contain such regions are at risk of initiating prion diseases.

“Amino acid sequence can tell us if a protein can potentially act as a prion and show prion-like functions,” said Vladimir Uversky, a professor at the University of South Florida specializing in molecular medicine. “Not all proteins with prion-like sequences will undoubtedly act as prions. Even prion protein itself will cause prion disease in very few cases.

“If, however, one got such proteins, then there is a chance that [the proteins] can trigger some pathology. It is not clear when, how, and with what probability this would happen, but the overall chances of getting something bad are definitely increased,” Mr. Uversky told The Epoch Times, comparing the prion protein to “a time bomb with a dysfunctional or stochastic timer.”


How Would mRNA Vaccines Form Prion Proteins?

One can think of mRNA vaccines as instructions used to make spike proteins. In the case of COVID-19 vaccines, the mRNA vaccines contain a high percentage of pseudouridine, which is less common in the human body. The extra pseudouridine makes the process more prone to “frameshift errors.”

Frameshift errors occur when the cell’s protein production machinery accidentally misses one or two bases in the mRNA sequence. Since mRNA bases are read in groups of threes, a frameshift breaks up the original sets of the sequence, affecting all sequences downstream of the error.

In his research, Mr. Perez found a frameshift by one base retains the prion-like sequences, while a frameshift by two bases eliminates them.

He also found that the frameshift sequences share similarities to bacterial proteins on the brain-eating amoeba and human nuclease proteins, proteins capable of breaking apart DNA bonds.


Spike Proteins and Prion Diseases in the Literature

Numerous papers in the literature have linked COVID-19 spike protein to prion formations.

The spike protein naturally has a prion-like domain at the region where it binds to other receptors.

SARS-CoV-2 is the only coronavirus with a prion-like domain in its spike protein.

In September 2023, Swedish researchers published a preprint finding that spike proteins may accelerate Alzheimer’s and prion disease formation.

The authors found specific spike protein sequences carried amyloid sequences and extracted them. When these sequences were supplemented with human prion and amyloid proteins, the spike sequences accelerated the proteins’ aggregation.

Neurologist Dr. Suzanne Gazda told The Epoch Times she is very concerned about the implications of prion disease acceleration and formation due to COVID-19 vaccination and infections.

Another study published in October 2023 found that spike protein can bind to alpha-synuclein, an unfolded protein that accumulates in Parkinson’s disease. The authors found that introducing spike protein to alpha-synuclein also increased its aggregation.


Several studies have linked COVID-19 and its vaccines with prion diseases.

A Turkish case study detailed the case of a 68-year-old man who developed symptoms of CJD weeks after being administered the COVID mRNA vaccine.

Around one to two weeks after administration, he became forgetful; two months later, he began losing his ability to find words. By the third to fourth month, he had developed a progressive speech disorder, confusion, agitation, and involuntary contraction of his left arm and leg.

A 2022 Italian case report examined the case of a man in his early 40s who developed CJD two months after a mild COVID-19 infection. He first started seeing black shadows when closing his eyes, “followed by dizziness, difficulty reading and worsening of balance,” the authors wrote.

Three months post-infection, the patient reported loss of coordination in his left arm and loss of reflexes in his legs.
 

Heliobas Disciple

TB Fanatic
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New long COVID study uncovers high inflammation in patients as Senate calls for more research on 'crisis'
ASHLEY RIEGLE - ABC News
Wed, January 24, 2024, 8:10 PM EST

A new study in Science is shining a light on the continuing impact of long COVID, with research revealing further and continuing health concerns for some of the 16 million sufferers in the U.S.

Long COVID is a syndrome, or collection of symptoms, that continue or develop after an acute COVID-19 infection and can last weeks, months or years. There is no test to confirm if symptoms are related to long COVID. Some scientists suggest that long COVID is caused by overactive immune cells, but the exact cause remains unclear.

The study followed 113 patients at four different hospitals in Switzerland with mild and severe COVID-19 and found that 40 had symptoms of long COVID at six months, 22 of whom had persistent symptoms at 12 months.

Researchers looked at blood samples from the 40 who experienced long COVID symptoms, compared them to controls who were not infected with COVID-19, and found that those who had long COVID had evidence of inflammation (increased complement activity), blood cell dysregulation (hemolysis and platelet activation) and tissue injury in their blood.

The specific details from the small study may help provide "a basis for new diagnostic solutions," according to the researchers, for the condition with no known cure or FDA-approved treatments.

While these results finding evidence of inflammation in patients with long COVID symptoms are not entirely surprising nor specific to long COVID, they are a step forward in identifying the cause of long COVID.

It's more than just researchers, though, looking into developments in our understanding of the syndrome. The condition received renewed attention from the federal government last week, as the U.S. Senate Committee on Health, Education, Labor and Pensions convened a group of patients and experts to testify about the impacts of long COVID before a bipartisan group of Senators.

In the Senate's first-ever hearing on this topic, Sen. Tammy Baldwin said researchers and government officials need to "increase the sense of urgency" over understanding and treating the condition.

For Sen. Bernie Sanders, chairman of the committee, more needs to be done.

"We think we haven't done anywhere near enough, and we hope to turn that around," he said.

Medical experts testified at the hearing, telling the committee that the condition can emerge in patients of all ages and backgrounds, that the risk increases with multiple infections, and rates of long COVID are higher in minority communities.

"The burden of disease and disability from long COVID is on par with the burden of cancer and heart disease," Dr. Ziyad Al-Aly, M.D., a clinical epidemiologist at Washington University, said. "We must develop sustainable solutions to prevent repeated infections with SARS-CoV-2 and long COVID that would be embraced by the public."


Patients and Caregivers


Angela Meriquez Vazquez, a long COVID patient from California, testified that she has helped over 15,000 sufferers through online advocacy.

"We are living through the largest mass destabilizing event in modern history," she told the Senators.

As she told her own story, Meriquez Vazquez, a former runner, said she is currently on 12 medications. Although she said she has managed to continue working, and she has health care, the condition has forced her to work from home, lying down to minimize her symptoms.

"Not since the emergence of the AIDS pandemic has there been such an imperative for large-scale change in healthcare, public health, and inequitable structures that bring exceptional risks of illness, suffering, disability, and mortality," Meriquez Vazzque said.

One of the Senators -- Republican Roger Marshall -- shared his own testimony, revealing to the committee that one of his loved ones "is one of the 16 million people" who has "suffered for two years" with the condition.

He told the committee his family member's illness is "like mono(nucleosis) that does not go away," adding that the person has seen 30 doctors in an attempt to find help.

Marshall said there needs to be more focus on treatments for long COVID at the Centers for Disease Control and Prevention.

"I'm frustrated that our CDC is more focused on vaccines than they are on treatments," he said.


Epidemiologists and Researchers weigh in

Dr. Al-Aly, while testifying, repeatedly called on our country's leaders and medical experts to come together to tackle the ongoing health crisis.

"We are the best nation on earth, and we can solve this," he said.

One of his proposed solutions is establishing a new multidisciplinary research institute to address infection-associated chronic conditions.

Research into the condition has been "slow," Dr. Charisse Madlock-Brown, Ph.D. from the University of Iowa, said at the hearing. She noted clinical trials are in the "experimental medicine" phase and pushed for more investment to identify proven treatments.

Sen. Tim Kaine said the National Institutes of Health has been provided more than $1 billion since 2020 to study long COVID, and he urged representatives from NIH to testify before the committee. In 2021, the NIH launched the Researching COVID to Enhance Recovery initiative to identify further risk factors and causes of long COVID.

"We can't take two years just to get 'geared up,'" he said.

According to the most recent information from the CDC, long COVID can cause up to 200 symptoms, including chronic fatigue, blood clots, gastrointestinal issues, brain fog and heart issues. Symptoms can last from months to years following a COVID infection. Risk factors for developing long COVID after a COVID-19 infection that have been identified include severe COVID-19 illness, underlying health conditions (such as asthma, diabetes, obesity or autoimmune diseases) and not getting the COVID-19 vaccine.

While the interest from the Senate and the new study in Science are promising, more research needs to be done to find the specific cause of why some people get long COVID from COVID-19, and others do not, and to find effective treatments.
 

Heliobas Disciple

TB Fanatic
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2 West Coast states are the first to depart from CDC's COVID isolation guidelines
Mary Walrath-Holdridge, USA TODAY
Wed, January 24, 2024, 5:46 PM EST

The remaining COVID-19 guidelines that still exist around the US are starting to fade away as we approach our fourth year of living with the pandemic.

Earlier this month, California's Department of Public Health issued a formal order to change existing COVID-19 control and prevention guidelines, reducing isolation expectations for infected individuals. The introduction of the new rules, which allow people testing positive to return to public life if they are not showing symptoms, makes California the second state to break from CDC guidelines and do away with specific isolation times, following behind Oregon, which made such changes back in May.

In California's order, issued on Jan. 9, the changes were attributed to the reduced impact of COVID compared to past years, the availability of treatment and the changing expectations to keep people most at-risk safe while posing minimal disruptions to the public.


Oregon and California limit quarantine

Oregon and California are the first states to depart from the guidelines put forth by the CDC, which still recommends at least five days of isolation after first testing positive for COVID or experiencing symptoms.

Instead, Oregonians and Californians are no longer asked to isolate for a specified period after contracting COVID. Those who experience symptoms can return to work or school after just 24 hours of being fever-free, so long as symptoms are "mild and improving." Those who experience no apparent symptoms are no longer required to isolate at all, according to the state policies.

However, both states still suggest taking precautions if you have been infected, even if you don't have to stay home anymore. It is still advised that you avoid contact with high-risk people and mask when around others for 10 days after testing positive or becoming sick.

“We are now at a different point in time with reduced impacts from COVID-19 compared to prior years due to broad immunity from vaccination and/or natural infection, and readily available treatments available for infected people,” Director of the California Department of Public Health Dr. Tomás Aragón said in the state order.

“Our policies and priorities for intervention are now focused on protecting those most at risk for serious illness while reducing social disruption that is disproportionate to recommendations for prevention of other endemic respiratory viral infections.?”


What does the CDC recommend?

The CDC guidelines still advise isolation with or without symptoms, regardless of vaccination status.

According to the guidelines, anyone who suspects they may have COVID-19 should begin isolating, even if they have not yet tested. Once testing positive, it is advised that you isolate for five days, as you are most likely to be contagious during that time.

If you test positive without symptoms but develop symptoms during the 10 days following, the isolation clock restarts. If at the end of the five days you are fever-free for 24 hours without the assistance of medication and your symptoms have improved, you may end isolation. However, if you are still experiencing symptoms with no improvement, you should wait until you are fever-free for 24 hours and/or your symptoms are improving.

People who experience more serious symptoms of shortness of breath or difficulty breathing should isolate for an additional five days, making the total quarantine time 10 days. People who had a severe illness that resulted in hospitalization or who are immunocompromised should consult their doctor about treatment plans and isolate for at least 10 days as well.

During isolation periods, the CDC suggests you:
  • Wear a high-quality mask if you must be around others at home and in public.
  • Do not go places where you are unable to wear a mask.
  • Do not travel.
  • Stay home and separate from others as much as possible.
  • Use a separate bathroom, if possible.
  • Take steps to improve ventilation at home, if possible.
  • Don’t share personal household items, like cups, towels, and utensils.
  • Monitor your symptoms. If you have an emergency warning sign (like trouble breathing), seek emergency medical care immediately.
 

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COVID survivors may be at a greater risk of developing Parkinson’s disease–like symptoms, researchers warn. What you need to know to protect your health
Erin Prater - Fortune
Wed, January 24, 2024, 12:04 PM EST

People who have been infected with COVID—yes, that’s virtually all of us—could be at greater risk for Parkinson’s disease–like symptoms down the line.

That’s according to a new study published this month in the journal Cell. Researchers from Weill Cornell Medicine, Memorial Sloan Kettering Cancer Center, and Columbia University used human stem cells to create cells from various organs, including the lung, heart, and pancreas. The virus was able to infect cells from all the aforementioned organs. But it did a particularly good job of infiltrating some types of neurons in the brain that produce dopamine—a neurotransmitter responsible for feelings of pleasure, motivation, memory, sleep, and movement.

Once infected, such cells can lose their ability to grow and divide, researchers found. The cells also stop producing dopamine and instead send out signals that cause inflammation.

Because a loss of dopamine-producing neurons is associated with Parkinson’s disease—a slowly developing neurodegenerative condition that leads to tremors and, often, dementia—people who’ve been infected with COVID are at an increased risk of developing symptoms of the disorder at some point in their lives, the researchers wrote.

“We keep discovering new cell types that can be infected by the virus,” Dr. Shuibing Chen, professor of chemical biology in surgery at Weill Cornell Medicine and lead author on the study, tells Fortune. “We’re still trying to understand how it damages them. We need to keep the work ongoing, keep watching to see what happens.”

Regardless, the virus’s detrimental effect on dopamine neurons may explain neurologic symptoms in those with an active COVID infection, like headache, loss of smell, and a persistent unpleasant taste in the mouth, according to researchers.

It may also explain more immediate neurologic symptoms of long COVID, like brain fog, sleep issues, depression, and anxiety.

However grim the findings, the team’s study resulted in some positive news: ALS drug riluzole, diabetes drug metformin, and cancer drug imatinib appear to prevent the aforementioned type of neurons from becoming infected with COVID and, thus, losing their ability to function properly.


COVID’s unknown future consequences


Chen’s research adds to a growing body of evidence that COVID may affect human health long after the initial infection—in ways that aren’t associated with stereotypical long COVID, and that aren’t yet well understood.

While there is no one agreed upon definition of long COVID, it’s generally defined as the continuation of COVID symptoms or development of new symptoms within three months of initial infection. Symptoms last at least two months—and years, potentially—with no other explanation.

Long COVID is thought to typically present as a chronic-fatigue-syndrome-like condition similar to other post-viral syndromes that can develop after an infection—with herpes, Lyme disease, Ebola, the flu, and other pathogens. Hundreds of additional long COVID symptoms have been identified, however, everything from the COVID-like—such as dry cough and shortness of breath—to the bizarre—like hallucinations, ear numbness, and a sensation of “brain on fire.”

Other post-COVID complications like long-term organ damage sustained during the virus’s acute phase should not be defined as long COVID and better fit under the larger umbrella category of PASC, or post-acute sequelae of COVID, some experts say.

Cellular damage, however, may not become apparent for months or years, as researchers are discovering. Aside from lung cells and some neurons, heart and colon cells can become infected with COVID, according to Chen, though the long-term implications are yet unknown.

What’s more, COVID can alter cells—perhaps permanently. Chen’s team discovered as much in 2021, when they found that COVID infiltrates the pancreas’s insulin-producing beta cells, causing them to secrete less insulin and to start making glucagon—a hormone that, in contrast with insulin, raises blood glucose levels.


Other viruses may also increase Parkinson’s risk

The jury is still out as to whether COVID poses a heightened risk of future disease, or if other viruses have similar but underappreciated effects on a host’s health.

It’s not the only virus that may lead to an increased future risk of developing Parkison’s Disease-like symptoms, Chen points out. The Spanish flu pandemic of 1917–1918 is thought to have had a similar effect, and other viruses might as well.

While the COVID pandemic was unfortunate, “it gave us a pretty unique opportunity to focus on studying a disease in a very short period of time,” she says. Many, if not most, other pathogens haven’t received such dedicated research focus. Thus, others might have similar effects.

As for whether everyone who’s been infected with COVID—pretty much all of us, by now—is at greater risk of eventually developing Parkinson’s-like symptoms, it’s tough to say, according to Chen. Multiple factors can contribute to disease development, including genetics; age; gender; a history of head trauma; exposure to chemicals like pesticides and herbicides; Vietnam-era exposure to Agent Orange; a history of working with heavy metals, detergents, and solvents—and, it appears, prior COVID infection.

Chen cautions that her team’s study was completed with cells grown in a lab—not in the complex environment of the human body. The findings, however, were corroborated by autopsies of those who had been infected with COVID before death.

Further study is needed, Chen says, to determine whether repeat COVID infection places people at a higher risk of Parkinson’s-like symptoms down the line, or increases the number of neurons damaged with each infection.

As for what the average person should do to protect their health, Chen advises decreasing the risk of COVID infection, whether that’s through masking or vaccination. The latter can limit the extent of infection—and perhaps the fallout from it—when a vaccinated person encounters the virus during daily life.

If a person who has experienced COVID begins to develop Parkinson’s disease symptoms, she recommends they inform their doctor of both their symptoms and the fact that their prior COVID infection could be placing them at higher risk of the disorder.

“It won’t hurt to keep that in mind,” she says.


What are the early symptoms of Parkinson’s disease?

While most people with Parkinson’s disease are diagnosed after age 60, 5% to 10% of patients with the condition begin to experience symptoms before age 50—some as early as 20.

The first symptom may be a minor tremor in just one hand—or even your finger or chin—while you’re resting. Here are some other early tells, according to the Parkinson’s Foundation:
  • Smaller handwriting than in the past
  • Loss of smell
  • Difficulty sleeping due to sudden involuntary movements
  • Arms that don’t swing when you walk like they used to
  • Stiffness in your arms, legs, or trunk
  • Constipation
  • A change in your voice that makes it very soft, breathy, or hoarse
  • A new lack of facial expression
  • Dizziness or fainting

As symptoms progress, people with Parkinson’s may find themselves experiencing more motor-related symptoms, like the following, according to the Cleveland Clinic:
  • Slow movements (these aren’t due to muscle weakness, but to muscle control problems, experts say)
  • Resting tremors
  • "Lead-pipe rigidity,” described as “constant, unchanging stiffness when moving a body part”
  • “Cogwheel stiffness,” which leads to a stop-and-go appearance of movements when lead-pipe rigidity is combined with tremors
  • Stooping or hunching over
  • Blinking less than usual
  • Drooling
  • Trouble swallowing

While there isn’t a cure for Parkinson’s, a variety of medications and treatments—like dopamine, medications that stimulate dopamine, medications like block dopamine metabolism, and deep-brain stimulation—can significantly improve symptoms.

There are experimental treatments, too, like stem cell transplants, neuron-repair treatments, gene therapies, and gene-targeted treatments, meaning more hope should be on the horizon for Parkinson's patients.
 

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How COVID-19 Vaccines and Infections Are Tweaking Our Immunity
Alice Park - TIME
Wed, January 24, 2024, 11:52 AM EST

Your immune system may be getting smarter every time you encounter COVID-19, a new study suggests. After getting vaccinated and infected, the immune system generates broader defenses against the virus, including against new variants.

In a paper published Jan. 19 in Science Immunology, researchers in South Korea compared immune cells in the lab from people with a variety of vaccine and infection histories throughout the different Omicron waves, which began in late 2021 with BA.1. People who had been vaccinated with the original Pfizer-BioNTech series and then got infected with any Omicron variant showed good levels of memory immune cells—called T cells—that defended not only against the variants causing the infection, but also related ones in the Omicron family that came later. For example, people who were vaccinated with three doses of the original COVID-19 shot and then got infected with the BA.2 variant generated T cells that could target not just BA.2 but also BA.4/5 and XBB viruses, which didn’t emerge until later.

“This is evidence of cross adaptation between the virus and human beings overall,” says Dr. Eui-Cheol Shin, professor at the Korea Advanced Institute of Science and Technology and senior author of the paper. “It also means we are on the way to an endemic era for COVID-19.”

Shin and his team found that the T cells—which are more durable than antibodies and are designed to retain memory of the viruses they encounter—generated against Omicron variants recognized the parts of the virus that remained conserved, as opposed to portions that had changed among the different variants. This, in part, helps people to not get as sick from reinfections.

The fact that the immune system is able to concentrate on these consistent parts of the virus could be an encouraging sign that the virus is evolving in a way to co-exist with humans, says Shin. There’s precedent for viruses becoming endemic in this way, since a handful of coronaviruses that started off as deadly now cause the common cold.

He and his team also found encouraging signs that the immune system may be gaining an edge over the virus. After you get a vaccine for any virus, immune cells tend to look for that version of the virus and are slower to generate defenses against different variants, making it easier for future versions of the virus to escape detection. Researchers thought COVID-19 vaccines would suffer a similar fate. People vaccinated with the initial two doses and booster shot of the vaccine that targeted the original virus, for example, were expected to generate weaker responses against future variants.

But Shin and his team found that people vaccinated with the original shot who then got infected with BA.2 still generated strong T-cell responses.

The study only includes data through the XBB wave. But Shin says he expects that the most recent vaccine, which targets XBB, would likely provide similar protection against the latest variants XBB and JN.1.

Reinfections aren't entirely benign. Other studies have shown that multiple bouts with the virus could raise the risk of long-term harm to the body in the form of Long COVID, which remains difficult to diagnose and treat.

Still, these findings suggest that the immune system is evolving to mitigate some of the more severe effects of COVID-19 infections—at least within the Omicron family of viruses. It’s not clear if and when SARS-CoV-2 might make a big genetic leap beyond Omicron, but for now, the combination of vaccines and natural infections is creating a hybrid immunity that seems to be keeping the virus under control for vaccinated people.
 

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What is COVID rebound? Doctors explain common symptoms and who's at risk
It's not clear exactly how common COVID rebound is or why it happens to some people and not others. Here's what we do know.

By Shiv Sudhakar, MD
Jan. 23, 2024, 5:29 PM UTC

With COVID levels high across most of the country, some people may find themselves experiencing symptoms of COVID rebound in the coming weeks.

“COVID rebound is a recurrence of COVID symptoms after initial improvement or a new positive test after a negative one,” Dr. Scott Roberts, associate medical director of infection prevention at Yale School of Medicine in New Haven, Connecticut, tells TODAY.com.

Earlier in the pandemic, COVID rebound was thought to be mostly caused by taking the antiviral treatment Paxlovid, as many of these patients would notice symptoms returning a few days after finishing treatment. But a recent report from the U.S. Centers for Disease Control and Prevention found no consistent link between taking Paxlovid and those who experienced COVID rebound.

Here’s a review on what we know so far about COVID rebound, as the U.S. continues to ride its second-largest COVID wave.

What is COVID rebound?

COVID rebound occurs when COVID symptoms stop and then return days later. It's not exactly clear why it happens.

The current evidence suggests COVID rebound usually occurs three to seven days after an infection resolves in patients, according to the December CDC report.

Here are some typical characteristics of COVID rebound:
  • Symptoms are usually mild.
  • You are unlikely to require hospitalization.
  • The illness lasts usually less than a week.
  • It is not specifically associated with Paxlovid.

Paxlovid was granted full approval in May 2023 by the U.S. Food and Drug Administration for adults 18 and older who have mild or moderate COVID and are high risk for severe disease. Research shows it can substantially reduce the risk of severe illness from COVID, including hospitalization and death.

It's prescribed to patients at high risk for complications to prevent them from getting so sick that they need to go to the hospital. Treatment lasts five days.

Who gets COVID rebound?

It's not clear exactly who will get COVID rebound, but it's possible that taking Paxlovid may increase your risk, Roberts notes.

“There is increasing evidence that rebound occurs in greater frequency in those taking Paxlovid compared to those without, although more data and more studies are needed for definitive answers to this question,” he explains.

In May 2022, the CDC alerted the public of reports of patients experiencing a recurrence of symptoms after stopping Paxlovid, usually within one week of discontinuing the medication. But when the FDA approved Paxlovid in May 2023, they noted rebound rates in clinical trials were similar among those who took the antiviral medication compared to those who took a placebo.

The CDC said in its December 2023 report that COVID rebound is “not associated specifically with receiving (Paxlovid).”

The report also noted that if you're high risk for severe illness from COVID — such as being immunocompromised or having underlying medical conditions — you may also be more likely to develop COVID rebound, but more research is needed.

President Joe Biden and first lady Jill Biden both experienced rebound after taking Paxlovid when they had COVID.

Why does COVID rebound happen?

“There is a lot of debate about why (COVID rebound) happens, but it is likely (the) natural disease course — rarely is it perfectly linear improvement — versus a result of taking Paxlovid,” Roberts says.

The CDC report also pointed to a "natural variability in viral dynamics" as one possible explanation for COVID rebound.

For patients who take Paxlovid, one theory is that it's so effective at suppressing the virus that the immune system lets the medication take over. So, when the medication has stopped, the immune system has to get back into the driver’s seat to fight the virus. As it gets to work and the immune response becomes more robust, you develop symptoms again.

But this theory doesn’t explain why some patients who are not on Paxlovid get rebound, too. One possible explanation is that in certain people, the immune system doesn't eliminate the infection early on and instead focuses on repairing the body, allowing the virus to continue to replicate and cause symptoms a second time.

How often does COVID rebound happen?

“Most people do not get rebound,” Roberts says. But it is difficult to know the exact number of people who get COVID rebound symptoms or test positive again after a negative test because many people who have rebound do not inform their doctors.

A Pfizer clinical trial estimated 2.3% of people who took Paxlovid experienced rebound compared to 1.7% of the control group, but other studies suggest the frequency is closer to 14% who took the antiviral compared to 9% who were not treated. One study from August 2022 that was not published in a peer-reviewed journal at the time found that COVID rebound could be as high as 27%.

Roberts estimates rebound occurs in about 1 in 5 people infected with COVID

How can you tell if you rebound?


If you test negative for COVID (after previously testing positive) and then develop symptoms and test positive again, that can be a sign of COVID rebound. Another way to tell that you have COVID rebound is if you start to feel worse again after feeling better, even without another positive test.

Symptoms of COVID rebound


The symptoms of COVID rebound are often mild similar to a cold:
  • Sore throat
  • Cough
  • Fatigue
  • Runny nose
  • Headache
  • Shortness of breath
  • Muscle aches
“In almost all cases the rebound event is much (milder) than the initial infection,” Roberts adds. Treatment typically isn't recommended for rebound symptoms.

How long does COVID rebound last?

COVID rebound symptoms and testing positive again usually last for about three days, according to the May 2022 health advisory from the CDC.

You may also be contagious during this time. "The CDC recommends a repeat isolation period, although it is very likely the degree of contagiousness is much less than the initial infectious episode,” Roberts says.

The CDC says people with COVID rebound symptoms should re-isolate for at least five days. End isolation once you are fever free for 24 hours without medication, if your symptoms are improving. And wear a mask for 10 days after rebound symptoms started.

Preliminary research suggests levels of the virus in the body are higher with rebound after Paxlovid compared to those who develop rebound without being on the treatment.

Is COVID rebound a reason not to take Paxlovid?

“If someone qualifies for Paxlovid, it is still in their best interest to take Paxlovid, even if there may be an increased risk of rebound,” Roberts stresses.

A recent National Institutes of Health study found only 15% of people who were eligible for the Paxlovid were prescribed the medication.Some providers who may be unfamiliar with a patient’s complete medical history, such as emergency room doctors and urgent care doctors, may be reluctant to prescribe the antiviral.

“Rebound is a small price to pay for the overwhelming benefits of taking Paxlovid in preventing high risk individuals from progressing to hospitalization, mechanical ventilation, and even death,” Roberts says.
 

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View: https://www.youtube.com/watch?v=Uq6cUHH4K1k
Navigating the Minefield of Spike Protein Detox
Vejon Health
Streamed live January 24, 2024
1 hr 23 min 57 sec

Discussion about the relevance of "Spike Protein Detox", is it even relevant and when should it occur.

Dr. Robin Rose, CEO and Founder of Terrain Health and Chief Medical Officer of MediCoreRx, is a double board-certified specialist in Gastroenterology and Internal Medicine, specializing in precision, functional medicine.

Dr Shankara Chetty is an internationally recognised family physician who used innovative techniques to protect his community from severe COVID-19.

Joachim Gerlach is co-founder of Vedicinals, focused on Research, Development and Production of novel therapeutics for infectious diseases as well as environmentally caused chronic illnesses.
 

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ht tps: // ww w. federal register. gov/documents/2023/12/21/2023-27935/institutional-review-board-waiver-or-alteration-of-informed-consent-for-minimal-risk-clinical
(fair use applies) DELIBERATELY BROKEN LINK

EXCERPT (I only posted the summary - the entire piece is at the link)

BOLDING MINE


~~~~~~~~~~~~~~~~~~~~~~~~~~~~~


This document has been published in the Federal Register. Use the PDF linked in the document sidebar for the official electronic format.


Publication Date:

12/21/2023


AGENCY:

Food and Drug Administration, HHS.

ACTION:

Final rule.

SUMMARY:

The Food and Drug Administration (FDA, the Agency, or we) is issuing a final rule to amend its regulations to implement a provision of the 21st Century Cures Act (Cures Act). This final rule allows an exception from the requirement to obtain informed consent when a clinical investigation poses no more than minimal risk to the human subject and includes appropriate safeguards to protect the rights, safety, and welfare of human subjects. The final rule permits an institutional review board (IRB) to waive or alter certain informed consent elements or to waive the requirement to obtain informed consent, under limited conditions, for certain FDA-regulated minimal risk clinical investigations.

DATES:

This rule is effective January 22, 2024.

[...]
 
Last edited:

psychgirl

Has No Life - Lives on TB
(fair use applies)


What is COVID rebound? Doctors explain common symptoms and who's at risk
It's not clear exactly how common COVID rebound is or why it happens to some people and not others. Here's what we do know.

By Shiv Sudhakar, MD
Jan. 23, 2024, 5:29 PM UTC

With COVID levels high across most of the country, some people may find themselves experiencing symptoms of COVID rebound in the coming weeks.

“COVID rebound is a recurrence of COVID symptoms after initial improvement or a new positive test after a negative one,” Dr. Scott Roberts, associate medical director of infection prevention at Yale School of Medicine in New Haven, Connecticut, tells TODAY.com.

Earlier in the pandemic, COVID rebound was thought to be mostly caused by taking the antiviral treatment Paxlovid, as many of these patients would notice symptoms returning a few days after finishing treatment. But a recent report from the U.S. Centers for Disease Control and Prevention found no consistent link between taking Paxlovid and those who experienced COVID rebound.

Here’s a review on what we know so far about COVID rebound, as the U.S. continues to ride its second-largest COVID wave.

What is COVID rebound?

COVID rebound occurs when COVID symptoms stop and then return days later. It's not exactly clear why it happens.

The current evidence suggests COVID rebound usually occurs three to seven days after an infection resolves in patients, according to the December CDC report.

Here are some typical characteristics of COVID rebound:
  • Symptoms are usually mild.
  • You are unlikely to require hospitalization.
  • The illness lasts usually less than a week.
  • It is not specifically associated with Paxlovid.

Paxlovid was granted full approval in May 2023 by the U.S. Food and Drug Administration for adults 18 and older who have mild or moderate COVID and are high risk for severe disease. Research shows it can substantially reduce the risk of severe illness from COVID, including hospitalization and death.

It's prescribed to patients at high risk for complications to prevent them from getting so sick that they need to go to the hospital. Treatment lasts five days.

Who gets COVID rebound?

It's not clear exactly who will get COVID rebound, but it's possible that taking Paxlovid may increase your risk, Roberts notes.

“There is increasing evidence that rebound occurs in greater frequency in those taking Paxlovid compared to those without, although more data and more studies are needed for definitive answers to this question,” he explains.

In May 2022, the CDC alerted the public of reports of patients experiencing a recurrence of symptoms after stopping Paxlovid, usually within one week of discontinuing the medication. But when the FDA approved Paxlovid in May 2023, they noted rebound rates in clinical trials were similar among those who took the antiviral medication compared to those who took a placebo.

The CDC said in its December 2023 report that COVID rebound is “not associated specifically with receiving (Paxlovid).”

The report also noted that if you're high risk for severe illness from COVID — such as being immunocompromised or having underlying medical conditions — you may also be more likely to develop COVID rebound, but more research is needed.

President Joe Biden and first lady Jill Biden both experienced rebound after taking Paxlovid when they had COVID.

Why does COVID rebound happen?

“There is a lot of debate about why (COVID rebound) happens, but it is likely (the) natural disease course — rarely is it perfectly linear improvement — versus a result of taking Paxlovid,” Roberts says.

The CDC report also pointed to a "natural variability in viral dynamics" as one possible explanation for COVID rebound.

For patients who take Paxlovid, one theory is that it's so effective at suppressing the virus that the immune system lets the medication take over. So, when the medication has stopped, the immune system has to get back into the driver’s seat to fight the virus. As it gets to work and the immune response becomes more robust, you develop symptoms again.

But this theory doesn’t explain why some patients who are not on Paxlovid get rebound, too. One possible explanation is that in certain people, the immune system doesn't eliminate the infection early on and instead focuses on repairing the body, allowing the virus to continue to replicate and cause symptoms a second time.

How often does COVID rebound happen?

“Most people do not get rebound,” Roberts says. But it is difficult to know the exact number of people who get COVID rebound symptoms or test positive again after a negative test because many people who have rebound do not inform their doctors.

A Pfizer clinical trial estimated 2.3% of people who took Paxlovid experienced rebound compared to 1.7% of the control group, but other studies suggest the frequency is closer to 14% who took the antiviral compared to 9% who were not treated. One study from August 2022 that was not published in a peer-reviewed journal at the time found that COVID rebound could be as high as 27%.

Roberts estimates rebound occurs in about 1 in 5 people infected with COVID

How can you tell if you rebound?

If you test negative for COVID (after previously testing positive) and then develop symptoms and test positive again, that can be a sign of COVID rebound. Another way to tell that you have COVID rebound is if you start to feel worse again after feeling better, even without another positive test.

Symptoms of COVID rebound

The symptoms of COVID rebound are often mild similar to a cold:
  • Sore throat
  • Cough
  • Fatigue
  • Runny nose
  • Headache
  • Shortness of breath
  • Muscle aches
“In almost all cases the rebound event is much (milder) than the initial infection,” Roberts adds. Treatment typically isn't recommended for rebound symptoms.

How long does COVID rebound last?

COVID rebound symptoms and testing positive again usually last for about three days, according to the May 2022 health advisory from the CDC.

You may also be contagious during this time. "The CDC recommends a repeat isolation period, although it is very likely the degree of contagiousness is much less than the initial infectious episode,” Roberts says.

The CDC says people with COVID rebound symptoms should re-isolate for at least five days. End isolation once you are fever free for 24 hours without medication, if your symptoms are improving. And wear a mask for 10 days after rebound symptoms started.

Preliminary research suggests levels of the virus in the body are higher with rebound after Paxlovid compared to those who develop rebound without being on the treatment.

Is COVID rebound a reason not to take Paxlovid?

“If someone qualifies for Paxlovid, it is still in their best interest to take Paxlovid, even if there may be an increased risk of rebound,” Roberts stresses.

A recent National Institutes of Health study found only 15% of people who were eligible for the Paxlovid were prescribed the medication.Some providers who may be unfamiliar with a patient’s complete medical history, such as emergency room doctors and urgent care doctors, may be reluctant to prescribe the antiviral.

“Rebound is a small price to pay for the overwhelming benefits of taking Paxlovid in preventing high risk individuals from progressing to hospitalization, mechanical ventilation, and even death,” Roberts says.
Very interesting article! Thank you for posting this. The topic is really helpful.
 

psychgirl

Has No Life - Lives on TB
:siren: :siren: :siren: :siren: :siren:



ht tps: // ww w. federal register. gov/documents/2023/12/21/2023-27935/institutional-review-board-waiver-or-alteration-of-informed-consent-for-minimal-risk-clinical
(fair use applies) DELIBERATELY BROKEN LINK

EXCERPT (I only posted the summary - the entire piece is at the link)

BOLDING MINE


~~~~~~~~~~~~~~~~~~~~~~~~~~~~~


This document has been published in the Federal Register. Use the PDF linked in the document sidebar for the official electronic format.


Publication Date:

12/21/2023


AGENCY:

Food and Drug Administration, HHS.

ACTION:

Final rule.

SUMMARY:

The Food and Drug Administration (FDA, the Agency, or we) is issuing a final rule to amend its regulations to implement a provision of the 21st Century Cures Act (Cures Act). This final rule allows an exception from the requirement to obtain informed consent when a clinical investigation poses no more than minimal risk to the human subject and includes appropriate safeguards to protect the rights, safety, and welfare of human subjects. The final rule permits an institutional review board (IRB) to waive or alter certain informed consent elements or to waive the requirement to obtain informed consent, under limited conditions, for certain FDA-regulated minimal risk clinical investigations.

DATES:

This rule is effective January 22, 2024.

[...]
Maybe this is worthy of its own thread?

I certainly think it is!
 

naegling62

Veteran Member
:siren: :siren: :siren: :siren: :siren:



ht tps: // ww w. federal register. gov/documents/2023/12/21/2023-27935/institutional-review-board-waiver-or-alteration-of-informed-consent-for-minimal-risk-clinical
(fair use applies) DELIBERATELY BROKEN LINK

EXCERPT (I only posted the summary - the entire piece is at the link)

BOLDING MINE


~~~~~~~~~~~~~~~~~~~~~~~~~~~~~


This document has been published in the Federal Register. Use the PDF linked in the document sidebar for the official electronic format.


Publication Date:

12/21/2023


AGENCY:

Food and Drug Administration, HHS.

ACTION:

Final rule.

SUMMARY:

The Food and Drug Administration (FDA, the Agency, or we) is issuing a final rule to amend its regulations to implement a provision of the 21st Century Cures Act (Cures Act). This final rule allows an exception from the requirement to obtain informed consent when a clinical investigation poses no more than minimal risk to the human subject and includes appropriate safeguards to protect the rights, safety, and welfare of human subjects. The final rule permits an institutional review board (IRB) to waive or alter certain informed consent elements or to waive the requirement to obtain informed consent, under limited conditions, for certain FDA-regulated minimal risk clinical investigations.

DATES:

This rule is effective January 22, 2024.

[...]
What does this mean?
 

Countrymouse

Country exile in the city
(fair use applies)


While Official Data Claims COVID-19 Cases Decreasing Nationwide, Hospitals In Massachusetts On Verge Of Collapsing
Nikhil Prasad Fact checked by:Thailand Medical News Team
Jan 24, 2024

Data from the U.S. CDC and from the new firm that the U.S. government has contracted for waste water surveillance i.e Verify…a company that belongs to Google!...claims that COVID-19 cases are declining nationwide, data from individual states and counties are showing the opposite.

In the state of Massachusetts, data shows that COVID-19 infections and hospital admissions were still high. From data released by the Massachusetts Department of Health, for the week 7th of January 2024 to 13th January 2024, there were a total of 41 COVID-19 deaths and there were 5491 COVID-19 cases.


However, for Emergency Department visits for various respiratory infections, a total of 63,323 visits were recorded for the same week.


It should be noted that the manner of reporting COVID-19 data by the Massachusetts government is devised to try to mislead anyone into understanding the actual COVID-19 scenario. They do not publish number of COVID-19 test conducted, the test posivity rates and actual COVID-19 hospital admissions.

However, latest COVID-19 News - United States updates are showing that various hospitals across the state are not only overwhelmed but also on the verge of collapsing.

Mass. General declares 'capacity disaster'


Massachusetts General Declares Code Help

Massachusetts General Hospital. One of the largest hospitals in the states has declared a "capacity disaster" as it grapples with an unprecedented crisis, requiring a significant increase in hospital beds to address a surplus of patients.

The situation, characterized by the hospital as a full-blown crisis, has persisted for the past 16 months, with the Emergency Department (ED) consistently operating at critical capacity levels. Patients are experiencing extended wait times for inpatient beds, with the ED frequently placed in a state of "Code Help" or "Capacity Disaster."

The crisis is exacerbated by the surge in illnesses such as COVID-19, flu, RSV, and other winter viruses. In a statement, a hospital spokesperson explained that "Code Help" occurs when inpatient beds and hallway stretchers are full, while "Capacity Disaster" is triggered when the ED reaches full capacity, all hallway stretchers are in use, and there are over 45 inpatients waiting for a hospital bed. Between October 2022 and September 2023, patients spent a total of 381,228 hours boarded in the hospital's ED, reflecting a 32 percent increase from the previous 12-month period.

In September alone, Mass. General saw patients boarding for a median of 14.1 hours, and 26 percent of admitted patients remained in the ED for more than 24 hours. Hospital President David F.M. Brown characterized the situation as a full-blown crisis for both emergency patients and healthcare workers, attributing it to the heightened demand for care in the post-pandemic era. Brown emphasized that 50 to 80 patients spend their first night of hospitalization in the ED daily, an inappropriate and non-therapeutic environment that significantly contributes to clinician burnout and frustration.

However, in the last three weeks, COVID-19 cases have exacerbated the situation to a point that the hospital directors are warning that the hospital services might simply collapse


View: https://twitter.com/MassGeneralNews/status/1748409540712812863


Mass. General is not alone in facing this challenge, as numerous hospitals in Massachusetts struggle with patient overflow. In response, hospitals statewide are prioritizing faster discharges to free up beds. Some health insurance providers have also agreed to waive prior authorizations that may delay patient discharge. The hospital has provided information on its response to the crisis on a dedicated webpage, urging the public to stay informed about the ongoing situation.

Other hospitals in Masschusetts like Beth Israel Deaconess Medical Center, Tufts Medical Center, Lahey Hospital and Medical Center and UMass Memorial Medical Center are all reporting almost similar situations with their ER departments being overwhelmed in the last 4 weeks and a shortage of COVID-19 beds.

The Massachusetts government has not made an official public announcement about the COVID-19 situation in the state or about what they are doing to deal with the situation.

Thailand Medical News will be providing more updates on the COVID-19 situation in Massachusetts.
Can we really rely on these reports, though? We read this when they began the last scare as well, but members who actually saw the hospitals (from inside) and various conservative reporting groups all said hospitals were empty and available.

Or are they full of IMMIGRANTS? (illegal)
 

Countrymouse

Country exile in the city
:siren: :siren: :siren: :siren: :siren:



ht tps: // ww w. federal register. gov/documents/2023/12/21/2023-27935/institutional-review-board-waiver-or-alteration-of-informed-consent-for-minimal-risk-clinical
(fair use applies) DELIBERATELY BROKEN LINK

EXCERPT (I only posted the summary - the entire piece is at the link)

BOLDING MINE


~~~~~~~~~~~~~~~~~~~~~~~~~~~~~


This document has been published in the Federal Register. Use the PDF linked in the document sidebar for the official electronic format.


Publication Date:

12/21/2023


AGENCY:

Food and Drug Administration, HHS.

ACTION:

Final rule.

SUMMARY:

The Food and Drug Administration (FDA, the Agency, or we) is issuing a final rule to amend its regulations to implement a provision of the 21st Century Cures Act (Cures Act). This final rule allows an exception from the requirement to obtain informed consent when a clinical investigation poses no more than minimal risk to the human subject and includes appropriate safeguards to protect the rights, safety, and welfare of human subjects. The final rule permits an institutional review board (IRB) to waive or alter certain informed consent elements or to waive the requirement to obtain informed consent, under limited conditions, for certain FDA-regulated minimal risk clinical investigations.

DATES:

This rule is effective January 22, 2024.

[...]
MERDE!

It means they can give you--without TELLING you they are giving it--the Covid shot, since they have declared it to be "safe"--and therefore of "no more than minimal risk to the human subject."
 

Countrymouse

Country exile in the city
(fair use applies)


COVID survivors may be at a greater risk of developing Parkinson’s disease–like symptoms, researchers warn. What you need to know to protect your health
Erin Prater - Fortune
Wed, January 24, 2024, 12:04 PM EST

People who have been infected with COVID—yes, that’s virtually all of us—could be at greater risk for Parkinson’s disease–like symptoms down the line.

That’s according to a new study published this month in the journal Cell. Researchers from Weill Cornell Medicine, Memorial Sloan Kettering Cancer Center, and Columbia University used human stem cells to create cells from various organs, including the lung, heart, and pancreas. The virus was able to infect cells from all the aforementioned organs. But it did a particularly good job of infiltrating some types of neurons in the brain that produce dopamine—a neurotransmitter responsible for feelings of pleasure, motivation, memory, sleep, and movement.

Once infected, such cells can lose their ability to grow and divide, researchers found. The cells also stop producing dopamine and instead send out signals that cause inflammation.

Because a loss of dopamine-producing neurons is associated with Parkinson’s disease—a slowly developing neurodegenerative condition that leads to tremors and, often, dementia—people who’ve been infected with COVID are at an increased risk of developing symptoms of the disorder at some point in their lives, the researchers wrote.

“We keep discovering new cell types that can be infected by the virus,” Dr. Shuibing Chen, professor of chemical biology in surgery at Weill Cornell Medicine and lead author on the study, tells Fortune. “We’re still trying to understand how it damages them. We need to keep the work ongoing, keep watching to see what happens.”

Regardless, the virus’s detrimental effect on dopamine neurons may explain neurologic symptoms in those with an active COVID infection, like headache, loss of smell, and a persistent unpleasant taste in the mouth, according to researchers.

It may also explain more immediate neurologic symptoms of long COVID, like brain fog, sleep issues, depression, and anxiety.

However grim the findings, the team’s study resulted in some positive news: ALS drug riluzole, diabetes drug metformin, and cancer drug imatinib appear to prevent the aforementioned type of neurons from becoming infected with COVID and, thus, losing their ability to function properly.


COVID’s unknown future consequences

Chen’s research adds to a growing body of evidence that COVID may affect human health long after the initial infection—in ways that aren’t associated with stereotypical long COVID, and that aren’t yet well understood.

While there is no one agreed upon definition of long COVID, it’s generally defined as the continuation of COVID symptoms or development of new symptoms within three months of initial infection. Symptoms last at least two months—and years, potentially—with no other explanation.

Long COVID is thought to typically present as a chronic-fatigue-syndrome-like condition similar to other post-viral syndromes that can develop after an infection—with herpes, Lyme disease, Ebola, the flu, and other pathogens. Hundreds of additional long COVID symptoms have been identified, however, everything from the COVID-like—such as dry cough and shortness of breath—to the bizarre—like hallucinations, ear numbness, and a sensation of “brain on fire.”

Other post-COVID complications like long-term organ damage sustained during the virus’s acute phase should not be defined as long COVID and better fit under the larger umbrella category of PASC, or post-acute sequelae of COVID, some experts say.

Cellular damage, however, may not become apparent for months or years, as researchers are discovering. Aside from lung cells and some neurons, heart and colon cells can become infected with COVID, according to Chen, though the long-term implications are yet unknown.

What’s more, COVID can alter cells—perhaps permanently. Chen’s team discovered as much in 2021, when they found that COVID infiltrates the pancreas’s insulin-producing beta cells, causing them to secrete less insulin and to start making glucagon—a hormone that, in contrast with insulin, raises blood glucose levels.


Other viruses may also increase Parkinson’s risk

The jury is still out as to whether COVID poses a heightened risk of future disease, or if other viruses have similar but underappreciated effects on a host’s health.

It’s not the only virus that may lead to an increased future risk of developing Parkison’s Disease-like symptoms, Chen points out. The Spanish flu pandemic of 1917–1918 is thought to have had a similar effect, and other viruses might as well.

While the COVID pandemic was unfortunate, “it gave us a pretty unique opportunity to focus on studying a disease in a very short period of time,” she says. Many, if not most, other pathogens haven’t received such dedicated research focus. Thus, others might have similar effects.

As for whether everyone who’s been infected with COVID—pretty much all of us, by now—is at greater risk of eventually developing Parkinson’s-like symptoms, it’s tough to say, according to Chen. Multiple factors can contribute to disease development, including genetics; age; gender; a history of head trauma; exposure to chemicals like pesticides and herbicides; Vietnam-era exposure to Agent Orange; a history of working with heavy metals, detergents, and solvents—and, it appears, prior COVID infection.

Chen cautions that her team’s study was completed with cells grown in a lab—not in the complex environment of the human body. The findings, however, were corroborated by autopsies of those who had been infected with COVID before death.

Further study is needed, Chen says, to determine whether repeat COVID infection places people at a higher risk of Parkinson’s-like symptoms down the line, or increases the number of neurons damaged with each infection.

As for what the average person should do to protect their health, Chen advises decreasing the risk of COVID infection, whether that’s through masking or vaccination. The latter can limit the extent of infection—and perhaps the fallout from it—when a vaccinated person encounters the virus during daily life.

If a person who has experienced COVID begins to develop Parkinson’s disease symptoms, she recommends they inform their doctor of both their symptoms and the fact that their prior COVID infection could be placing them at higher risk of the disorder.

“It won’t hurt to keep that in mind,” she says.


What are the early symptoms of Parkinson’s disease?

While most people with Parkinson’s disease are diagnosed after age 60, 5% to 10% of patients with the condition begin to experience symptoms before age 50—some as early as 20.

The first symptom may be a minor tremor in just one hand—or even your finger or chin—while you’re resting. Here are some other early tells, according to the Parkinson’s Foundation:
  • Smaller handwriting than in the past
  • Loss of smell
  • Difficulty sleeping due to sudden involuntary movements
  • Arms that don’t swing when you walk like they used to
  • Stiffness in your arms, legs, or trunk
  • Constipation
  • A change in your voice that makes it very soft, breathy, or hoarse
  • A new lack of facial expression
  • Dizziness or fainting

As symptoms progress, people with Parkinson’s may find themselves experiencing more motor-related symptoms, like the following, according to the Cleveland Clinic:
  • Slow movements (these aren’t due to muscle weakness, but to muscle control problems, experts say)
  • Resting tremors
  • "Lead-pipe rigidity,” described as “constant, unchanging stiffness when moving a body part”
  • “Cogwheel stiffness,” which leads to a stop-and-go appearance of movements when lead-pipe rigidity is combined with tremors
  • Stooping or hunching over
  • Blinking less than usual
  • Drooling
  • Trouble swallowing

While there isn’t a cure for Parkinson’s, a variety of medications and treatments—like dopamine, medications that stimulate dopamine, medications like block dopamine metabolism, and deep-brain stimulation—can significantly improve symptoms.

There are experimental treatments, too, like stem cell transplants, neuron-repair treatments, gene therapies, and gene-targeted treatments, meaning more hope should be on the horizon for Parkinson's patients.
I remember reading early on, after they first rolled out the shots, that one of the early and almost-immediate side effects was Parkinsons in people who'd never had any symptoms before.
 

naegling62

Veteran Member
Can we really rely on these reports, though? We read this when they began the last scare as well, but members who actually saw the hospitals (from inside) and various conservative reporting groups all said hospitals were empty and available.

Or are they full of IMMIGRANTS? (illegal)
My brother was the guy putting the patients on the respirators. At his hospital the COVID wards were full. My daughter in law was a phlebotomist at a hospital in Birmingham, they had numerous floors dedicated to COVID patients that were full.

* 2020-2021.
 
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psychgirl

Has No Life - Lives on TB
My brother was the guy putting the patients on the respirators. At his hospital the COVID wards were full. My daughter in law was a phlebotomist at a hospital in Birmingham, they had numerous floors dedicated to COVID patients that were full.
Same report from my niece.
She’s at a hospital working the night shift as an orderly. That hospital (central Indiana) was completely full Thanksgiving weekend.
It’s been full every season since Covid began. She did say that this year they also have a lot of RSV patients too.
 
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