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Two influenza A viruses, neurotropic nws and its recombinant nw are capable of forming plaques on BHK21 cells, nws plaques are larger than nw plaques. The small plaque size of nw virus is related to a slower rate of increase of nw than nws virus during many cycles of infection, not to inhibition by the non-cellular environwent. The slow increase could be accounted for by a delay in the formation of infectious nw virus in each cycle accompanied by a simultaneous delay in release. The synthesis of nw virus is accompanied by a large quantity of unassembled or unstable noninfectious haemagglutinin; the synthesis of nws virus yields assembled infectious haemagglutinin predominantly.
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