Figure 1.

Mutation and reassortment giving rise to antigenic drift and antigenic shift in different hosts of influenza virus. The surface hemagglutinin and neuraminidase molecules (blue) of influenza viruses, which play an essential part in viral recognition of and entry into host cells, undergo frequent mutation (antigenic drift) in their human hosts, giving rise to new variants (red dots) that can elude antibodies made in many individuals against the parent virus. Less frequently, entire segments of the eight-segment genome of an avian influenza virus and a human virus become reassorted into the same virion, usually through infection of swine by both viruses, and this can result in a virus that is still adapted to infect humans but expresses an avian hemagglutinin or neuraminidase (antigenic shift) to which there is no prior immunity in human populations. These give rise periodically to pandemics. Figure reproduced with permission from Figure 10-17 of: DeFranco AL, et al. 2007 [24].

Turner et al. BMC Biology 2010 8:130   doi:10.1186/1741-7007-8-130
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