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Untitled - D Ank Unlimited

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influenza virus immunity 390 influenza virus immunity<br />

Influenza virus.<br />

HA<br />

NA<br />

PB2 PB1PA NP<br />

Influenza A subtype N2 neuraminidase (sialidase). A/Tokyo/3/67.<br />

M1<br />

0<br />

nm<br />

M2<br />

NS 1 and NS 2<br />

50<br />

Influenza B/LEE/40 neuraminidase (sialidase).<br />

the NA are in a central cavity encircled by two antigenic<br />

sites. Influenza A viruses undergo variability that includes<br />

antigenic drift, which yields variants of contemporary<br />

epidemic strains that are sufficiently different to avoid<br />

neutralization by antibody. The more extensive antigenic<br />

shift may be a consequence of dual infection with human<br />

and animal influenza A viruses. This can lead to the<br />

development of a novel pandemic strain for which humans<br />

have no preexisting antibodies. CD8 + virus-immune<br />

cytotoxic T lymphocytes can clear influenza A virus from<br />

infected lungs. It is necessary for the effector lymphocyte<br />

to come into direct contact with the virus-infected target<br />

cell. Immune CD4 + T lymphocytes are involved in lung<br />

consolidation in influenza pneumonia and have a significant<br />

role in clearance of the virus. CD4 + T cells facilitate<br />

antibody production. They also facilitate the generation<br />

of “helper cytokines” such as interleukin-4 (IL4) and<br />

IL5 that promote clonal expansion and differentiation of

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