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Chapter 16.14 : Avian Influenza

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Avian Influenza, Page 1 of 2

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Abstract:

Influenza A virus is a member of the family Influenza viruses are enveloped, with a segmented, singlestranded RNA genome. This family also contains influenza B and C viruses. Point mutations in the envelope protein hemagglutinin (H), referred to as antigenic drift, result in the emergence of new strains of influenza A and B viruses and the resultant annual outbreaks and epidemics. New influenza A virus subtypes emerge as the result of reassortment of H and neuraminidase (N) sequences from two different subtypes, referred to as antigenic shift. These new subtypes are responsible for influenza pandemics. There are currently 16 recognized H subtypes and 9 recognized N subtypes. While virtually all combinations of influenza A subtypes naturally infect waterfowl and shorebirds, certain subtypes infect poultry and mammalian species. Subtypes H1N1, H3N2, H2N2, and H1N2 have circulated, or are currently circulating widely, among humans. Subtype H5N1, causing highly pathogenic avian influenza, was identified in 1996 in southern China. Influenza A H5N1 is significant, though not unique, in its ability to cross normal species barriers and directly infect humans; avian subtypes H9N2 and H7N7 are also known to cause infection in humans. For this reason, testing for H5N1 virus alone is not recommended, and any unusual influenza viruses that cannot be subtyped should be referred to a public health laboratory or the CDC. Among pathogenic avian influenza virus strains, the wide geographical distribution of H5N1 in avian species and the number and severity of human infections are unprecedented. If, or when, the virus evolves into a strain transmitted readily among humans, and unless there is a dramatic decrease in the pathogenicity of the resulting virus, the result will likely be an influenza pandemic with mortality rates not seen since the 1918 pandemic.

Citation: Garcia L. 2010. Avian Influenza, p 835-841. In Clinical Microbiology Procedures Handbook, 3rd Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817435.ch16.14
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References

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