Mode of replication of lymphocytic choriomeningitis virus in persistently infected cultivated mouse L cells.

During persistent infection of mouse L cells with strain Armstrong lymphocytic choriomeningitis virus, the latter undergoes characteristic changes, including loss of mouse pathogenicity and failure to form plaques on cultivated cells. We call this virus L(Arm) and have analyzed transcription and translation of its S-RNA, which codes for the viral nucleoprotein (NP) and the glycoprotein precursor (GP-C). In L(Arm) virus-infected L cells, S-RNA and genomic-sized viral complementary S-RNA (VC-S-RNA) were detected and, in addition, considerable quantities of shortened molecules of either species. The cells' content of NP was high, but they contained little GP-C; instead, a viral glycoprotein with MW 65,000 was present. We propose a hypothesis in which it is assumed that along the VC-S-RNA there is more than one recognition site for the viral RNA-dependent RNA polymerase, which leads to the generation of truncated forms of S-RNA, VC-S-RNA, and mRNA for GP-C; this, in turn, results in relative overproduction of NP and relative underproduction of GP-C as well as the emergence of a new form of viral glycoprotein.