With regard to molecular epidemiology, influenza A viruses belong to the best-studied virus systems. At least two large reservoirs of influenza A viruses have been built up in nature, one in humans and another one in water fowls. The latter one is very heterogenous, consisting of viruses belonging to 13 hemagglutinin (HA) and 9 neuraminidase (NA) subtypes in almost all possible combinations. The segmented structure of the influenza virus genome allows the creation of new influenza strains by reassortment. By replacement of the HA gene of human strains new pandemic viruses can be generated (antigenic shift). The particular structure of the HA enables the human influenza A-viruses to create variants which can escape the immune response of the host (antigenic drift). The nucleoprotein is responsible for keeping those two large reservoirs apart. Mixing of genes of viruses from these two reservoirs seems to happen predominantly by double infection of pigs, which apparently are tolerant for infection by either human or avian influenza viruses. The molecular mechanisms described for influenza viruses can be explained by the particular structure of their genome and their components and cannot be generalized. Each virus has developed its own strategy to multiply and to spread.
Key wordsEpidemiology of influenza antigenic drift antigenic shift virus reservoirs reassortment
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- 2.Gammelin, M., et al., manuscript in preparation.Google Scholar
- 3.Geraci, R., St. Aubin, D. J., Barker, I. K., Webster, R. G., Hinshaw, V. S., Bean, W. J., Ruhnke, H. L., Prescott, J. H., Early, G., Baker, V. S., Madoff, S., and Schooly, R. T., Mass mortality of harbor seals: Pneumonia associated with influenza virus. Science215 (1982) 1129–1131.PubMedGoogle Scholar
- 5.Hinshaw, V. S., Bean, W. J., and Webster, R. G., Biologic and genetic characterization of an influenza A virus associated with epizootie pneumonia in seals, in: Genetic Variation among Influenza Viruses, pp. 515–524. Ed. D. P. Nayak. Academic Press, New York-London-Toronto-Sydney-San Francisco 1981.Google Scholar
- 8.Kistner, O., et al., manuscript in preparation.Google Scholar
- 9.Klenk, H.-D., and Rott, R., Cotranslational and posttranslational processing of viral glycoproteins. Curr. Top. Microbiol. Immun.90 (1980) 19–48.Google Scholar
- 11.Reinacher, M., Bonin, J., Narayan, O., and Scholtissek, C., Pathogenesis of neurovirulent influenza A virus infection in mice. Route of entry of virus into brain determines infection of different populations entry of virus into brain determines infection of different populations of cells. Lab. Invest.49 (1983) 686–692PubMedGoogle Scholar
- 14.Scholtissek, C., The genome of the influenza virus. Curr. Top. Microbiol. Immun.80 (1978) 139–169.Google Scholar
- 18.Scholtissek, C., Vallbracht, A., Flehmig, B., and Rott, R., Correlation of pathogenicity and gene constellation of influenza A viruses. II. Highly neurovirulent recombinants derived from non-neurovirulent or weakly neurovirulent parent virus strains. Virology95 (1979) 492–500.CrossRefPubMedGoogle Scholar