Is H7N9 Spreading from Human to Human in China?
H5N2 outbreak - not found in rodents or wild birds
http://www.jstor.org/discover/10.230...21102161564147
However, this second study has a number of interesting points in the discussion.
http://www.plosone.org/article/info%...l.pone.0039206
Low-Pathogenic Avian Influenza Viruses in Wild House Mice
Discussion
This study provides evidence that avian influenza viruses may be naturally transmitted to mice at outbreak sites and that wild house mice can efficiently replicate avian influenza viruses without prior adaptation. Even though our sample size was low and we were sampling nearly a month after the outbreak was first detected, the house mice in our mammal survey at the Idaho outbreak site showed a positive response for influenza A antibodies. We recommend that future outbreaks allow for significant rodent sampling on the premises as soon as an outbreak is detected to further our understanding of the role rodents may play in avian influenza dynamics at outbreak sites. Furthermore, low sera sample volumes for the mice prevented us from subtyping the samples, which may have provided stronger support for past avian influenza virus infection. The ELISA used in this study was type-specific for antibodies to influenza A; therefore we cannot rule out that the mice may have been infected with a mammalian influenza strain rather than an avian strain. However, the outbreak farm housed only birds so the probability of the presence of a mammalian influenza strain was likely to be lower than for an avian strain.
Few studies have explored the seroprevalence of avian influenza viruses in synanthropic wildlife at outbreak sites and active areas of infection. Exceptions are surveys by Nettles et al. [55], Henzler et al. [56], and Shortridge et al. [57]. In the first study more than 250 mice and rats from infected farms were sampled after a 1983–84 outbreak of H5N2 virus in domestic poultry in the eastern U.S. No evidence for influenza infection was found in the rodents. However, rodent sampling was conducted 2–3 months post-outbreak, which is relatively late given the monthly survival rate of mice on farms can be as low as 0.55 [58]. Henzler et al. also surveyed mice on poultry farms during an outbreak of H7N2 in poultry in Pennsylvania, U.S. from 1996–1998. Lung and intestinal tissues were tested by virus isolation and all samples were found to be negative. In the Shortridge et al. study, mice and rats associated with poultry markets in Hong Kong were surveyed for exposure to avian influenza viruses after the initial detection of Asian strain H5N1 virus. Again, no virus was isolated from either rodent species, but rats showed evidence of hemagglutination inhibition activity and the ability of both mice and rats to replicate the H5N1 virus was subsequently confirmed [30].
A potential caveat with regard to mammalian sero-surveys is that many assays developed to detect antibodies to avian influenza viruses are optimized for poultry species and may not be validated for other species. Consequently, assay sensitivity and specificity may not be consistent with published parameters. Further, a number of commercial enzyme-linked immunosorbent assays (ELISAs) developed for detection of antibodies to avian influenza viruses use anti-mouse antigens and may not be appropriate for rodents. Hemagluttination inhibition (HI) tests may also be problematic as mouse sera may cause non-specific binding that interferes with HI tests [59]. Only a third of the mice tested in this study were positive for antibodies to avian influenza virus. Further work needs to be done to elucidate whether mice lacking an ELISA response would be protected upon re-exposure to influenza virus.
Rodents could contribute to avian influenza virus transmission on and among farms in a number of ways. Mice and rats could spread virus via mechanical transmission [60]. Alternatively, they could contribute to viral spread by becoming infected via scavenging on infected poultry carcasses [2] or by contact with contaminated water sources [61] and subsequently transmitting virus if they are scavenged or predated. Mice are a very common prey species for a variety of raptors, meso-predators, and other mammalian carnivores and are also commonly eaten by barnyard chickens. The high concentrations of viral RNA detected in the lungs of experimentally infected house mice indicate that wild mice may have the potential to replicate sufficient virus for transmission to other species.
We tested five subtypes of avian influenza virus in order to compare the replication potential of subtypes derived from both wild birds and chickens. Our results indicate that wild mice were able to more efficiently replicate viruses originating from wild birds than from poultry. Viral RNA was detected in 94% of lung, 86% of nasal turbinate, and 78% of trachea tissues from mice inoculated with wild bird viruses compared with 51% of lung, 44% of nasal turbinate, and 20% of trachea tissues from mice inoculated with chicken viruses. Given the wide range of replication potential for different avian influenza virus subtypes and different strains within subtypes, this pattern of higher viral replication of wild bird viruses compared with poultry viruses may be due to chance. Further study is needed to confirm this general result, but if the pattern holds, it may indicate that mice are more likely to introduce an avian influenza strain from wild birds to poultry than to spread poultry viruses among and between farms.
Studying wild house mice rather than laboratory mice is essential to understanding the potential role that mice may play in avian influenza virus outbreak dynamics because wild house mice and laboratory mice may exhibit differential immune function [42]. Standard laboratory mice, including BALB/c mice, have a defective Mx1 gene (Mx1−) that reduces their ability to resist influenza virus infections [62], [63], [64], [65]. On the other hand, wild mice with an intact Mx1 gene (Mx1+) are resistant to influenza virus infection [63], [64]. Consequently, the results of studies based on experimental infections of laboratory mice may not accurately reflect viral replication in wild mice. In addition to differing genetics, natural populations of wild mice are likely to include a broad spectrum of heterogeneities that might influence viral replication. For example, sex, age, reproductive status, behavior, nutritional condition, disease status, and parasite load are all likely to affect immune function [42], [43], [66]. In this study, wild house mice were fed standard laboratory diets for 2–5 weeks prior to testing and were dusted for parasites, so individual differences due to nutritional status or parasite loads were likely diminished. However, we were able to evaluate sex and found that female mice exhibited higher viral replication rates compared to males. While none of the females in this study were pregnant at the time of inoculation, a few individuals gave birth during the quarantine period and a range of hormonal conditions were likely. Previous studies of influenza in mice indicate that morbidity, mortality, and viral loads are higher for pregnant females compared with non-pregnant controls [67], [68]. Differential replication rates may be important to consider in the development of risk assessment and transmission models because individuals with higher viral loads may be more likely to cause an infection post contact with a potential host. If so, the basic reproductive number, or the mean number of secondary infections caused by an infected individual, may be different for males and females and that difference might be important in epidemiologic models.
In summary, the ability of wild mice to efficiently replicate avian influenza viruses without adaptation indicates the potential role of wild house mice in avian influenza virus outbreak dynamics and warrants further investigation. In particular, studies that seek to confirm the presence of avian influenza virus antibodies, detect virus, or examine the ability of mice to transmit virus to other species would shed light on whether or not rodent control is an important strategy for avian influenza virus outbreak control.
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Where I got this article:
http://www.flutrackers.com/forum/showthread.php?p=493741
I was really hoping it wouldn't be rats / mice. Of all the things that could carry it, that would be about the worst.