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Every year, influenza causes epidemic disease. Periodically, antigenic drift and shift enable influenza viruses to evade human immunity from prior seasons, increasing the severity of the associated illnesses. Since the 1918 pandemic, circulating influenza A viruses have had several antigenic shifts, resulting, for example, in the emergence of the A/H2N2 (1957–1958) and A/H3N2 (1968–1969) strains, but influenza more often drifts with modest antigenic changes.1,2 A recent analysis has shown that a few specific point mutations near the hemagglutinin-receptor binding site of A/H3N2 and both circulating B lineages (B/Yamagata and B/Victoria) allow evasion of immunity.2 A central part of the . . .
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Lindsey R. Baden (2013) studied this question.
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