FIGURE 2 | Known mechanisms for the emergence of pandemic influenza A virus strains.

From the following article:

Glycan microarray technologies: tools to survey host specificity of influenza viruses

James Stevens, Ola Blixt, James C. Paulson & Ian A. Wilson

Nature Reviews Microbiology 4, 857-864 (November 2006)

doi:10.1038/nrmicro1530

Glycan microarray technologies: tools to survey host specificity of influenza viruses

Two of the three pandemic influenza A virus strains during the past century, H2N2 in 1957 (which caused Asian flu) and H3N2 in 1968 (which caused Hong Kong flu), arose from genetic reassortment, in which gene segments from an avian virus were mixed with genetic material from a co-infecting human virus, probably through an intermediate host, such as a pig (the mixing vessel theory). The haemagglutinin (HA) of human influenza A viruses has a binding preference for cell receptors that contain alpha2-6-linked sialic-acid moieties, whereas avian viruses bind preferentially to alpha2-3-linked sialic acids moieties. The respiratory epithelial cells of pigs have receptors that express both alpha2-3- and alpha2-6-linked sialic-acid moieties, and can be infected by both human and avian viruses. The resulting viral progeny will either be intact avian or human virus, which can only infect their respective hosts or, if reassortment yields functional virus (usually swapped HA, PB2 and/or neuraminidase (NA)), a new pandemic strain might emerge with the ability to retain efficient human-to-human transfer, but be sufficiently different (for example, by a species change in HA) to reduce the ability of the host to mount an effective immune response. PB2, polymerase basic-2 protein.

Download file

If the slide opens in your browser, select "File > Save As" to save it.