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| Antigenic variation in influenza comes in a multitude of forms,
enabling it to effectively evade the immune system. As with all RNA viruses, the influenza
virus lacks a proofreader for replication, allowing the virus to mutate quickly. The host
immune system selects for mutants by making antibodies to the original strain of virus.
This leads to antigenic drift, whereby the virus slowly changes its form. In humans,
changes in certain genes can lead to increasing virulency. Interestingly, antigenic drift
in avian influenza is at a standstill; mutant viruses contain only silent changes in amino
acid sequences. Influenza viral genes are carried on different segments: Influenza A and B both have 8 segments, while C has only 7. The virus is able to reassort its genes, swapping parts and whole segments of the virus in co-infected cells. Co-infection can also lead to complementation, whereby segments of one viral strain can replace nonfunctional segments of other strains. |
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Of the three influenza strains, only A appears to infect humans and
animals (birds, swine, horses and seals). Influenza strains are usually species specific,
yet both avian and human influenza strains can infect swine. If cells in the pig are
co-infected with human and avian virus, reassortment can lead to major changes in the
make-up of the virus. This is called antigenic shift, whereby a sudden dramatic change in
the viral genome occurs. Major epidemics and pandemics have occurred when either or both
of the two major surface glycoproteins, hemagglutinin (HA) and neuraminidase (NA), from
birds recombined with other human segments. |
| HA functions in cell recognition and attachment to host cells. Point mutations in HA antigenic sites can result in variants that evade the host immune system. The other major surface antigen, NA, acts to release viral particles from the infected cells. Both NA and HA have subtypes which account for the diversity of influenza strains. |
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 All human influenza epidemics since 1930 have originated in China. In 1957, Asian flu acquired 3 genes (segments with hatched bars) by reassortment from Eurasian avian viruses and kept 5 gene segments from circulating human strains (black bars). In 1968, Hong Kong flu acquired 2 genes (white bars) by reassortment from Eurasian avian viruses and kept 6 gene segments from circulating human strains (black bars). ( Adapted from Webster R.G. et al.) |
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