Abstract
Influenza Al/CAM virus undergoes abortive growth in FL cells, whereas X-3311, a recombinant virus clone from the cross between CAM and NWS, is capable of complete replication in FL cells and plaque formation on FL monolayers (FL-marker). Clone 1-5C-4 cells are permissive for both viruses. When either clone 1-5C-4 or FL cells, which were mixedly infected with both ultraviolet-irradiated X-3311 and active CAM viruses, were plated on FL monolayers, infective centers far exceeding in number those expected from the surviving X-3311 virus were observed, i.e., the FL-marker of the irradiated parent was rescued. The significantly lower radiation sensitivity of FL-marker than that of infectivity indicates that only part of the genome is responsible for the FL-marker. The capability of X-3311 virus to produce NP antigen and its infectivity were lost at the same time when the former was assayed under the condition of low multiplicity of infection. This suggests that only infectious virus is capable of producing NP antigen and that no stepwise inactivation of the viral genome occurs. It is also suggested that any lethal ultraviolet damage inflicted upon the viral genome prevents the expression of the portion of the genome coding for NP antigen.
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