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Review
. 2008 Jan;41(1):1-6.
doi: 10.1016/j.jcv.2007.10.017.

Emerging influenza

Emmie de Wit  1 , Ron A M Fouchier
Affiliations
Review

Emerging influenza

Emmie de Wit et al. J Clin Virol. 2008 Jan.

Abstract

In 1918 the Spanish influenza pandemic, caused by an avian H1N1 virus, resulted in over 50 million deaths worldwide. Several outbreaks of H7 influenza A viruses have resulted in human cases, including one fatal case. Since 1997, the outbreaks of highly pathogenic avian influenza (HPAI) of the H5N1 subtype have affected a wide variety of mammals in addition to poultry and wild birds. Here, we give an overview of the current knowledge of the determinants of pathogenicity of these three subtypes of avian influenza A virus in mammals. Common mechanisms for acquisition of virulence and replication of these avian influenza viruses in mammals are becoming apparent. Therefore, monitoring these and additional genetic changes upon zoonotic infections is important. Identification of genetic changes responsible for transmission between mammals will be an important task for the near future.

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Figures

Figure 1
Figure 1
Determinants of avian influenza virus pathogenicity in mammals. 1. HA of influenza A virus is important for receptor binding, fusion and entry into the host cell. HA of avian viruses preferentially bind to α-2,3-linked SA, whereas human viruses preferentially bind to α-2,6-linked SA. 2. The influenza virus polymerase complex undergoes changes to facilitate replication in the mammalian host cell. 3. Virus replication results in an innate immune response to block virus replication. The NS1 protein is able to antagonize this response and modulate production of proinflammatory cytokines and chemokines. 4. NA is essential for the release of virus particles from the infected cell and thus for spread of the virus by destroying α-2,3-and α-2,6-linked SA receptors.
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