SUMMARY

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