SUMMARYThe virus-induced polypeptides synthesized in human embryonic lung cells infected with ts4, a DNA negative temperature-sensitive mutant of herpes simplex virus type I, were examined at the permissive (34 °C) and non-permissive (39 °C) temperatures using SDS-polyacrylamide gel electrophoresis. Cells infected with ts4 at 34 °C synthesized virus-specific polypeptides in the same proportion as did wild-type-infected cells at 34 and 39 °C. Cells infected with ts4 at 39 °C exhibited multiple polypeptide defects, the most prominent of which was the inhibition of the synthesis of the major virus capsid polypeptide, VPI54. The expression of the temperature-sensitive defect relating to VPI54 only occurred prior to 4 h after infection, as shown by shift-up studies. The expression of the temperature-sensitive defect at 39 °C relating to VPI54 could be reversed by shifting down infected cells to 34 °C, even after ia h at the non-permissive temperature. This reversal occurred in the presence of cytosine arabinoside but not in the presence of actinomycin D.

Temperature-sensitive mutants of herpes simplex virus type 1 belonging to four DNAcomplementation groups exhibited two distinct patterns of viral DNA synthesis after shift-up to the nonpermissive temperature. In cultures infected with mutants belonging to complementation groups A, C, and D, little or no viral DNA was synthesized after shift-up. In cultures infected with a mutant in complementation group B, nearly normal amounts of viral DNA were synthesized after shiftup.

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Temperature-sensitive mutants of herpes simplex virus type 1 representing eight DNA-negative complementation groups were grouped into the following three categories based on the viral DNA synthesis patterns after shift-up from the permissive to the nonpermissive temperature and after shift-down from the nonpermissive to the permissive temperature in the presence and absence of inhibitors of RNA and protein synthesis. (i) Viral DNA synthesis was inhibited after shift-up in cells infected with tsB, tsH, and tsJ. After shift-down, tsBand tsH-infected cells synthesized viral DNA in the absence of de novo RNA and protein synthesis whereas tsd-infected cells synthesized no viral DNA in the absence of protein synthesis. The B, H, and J proteins appear to be continuously required for the synthesis of viral DNA. (ii) Viral DNA synthesis continued after shift-up in cells infected with tsD and tsK whereas no viral DNA was synthesized after shift-down in the absence of RNA and protein synthesis. Mutants tsD and tsK appear to be defective in early regulatory functions. (iii) Cells infected with tsL, tsS, and tsU synthesized viral DNA after shift-up and after shift-down in the absence of RNA and protein synthesis. The functions of the L, S, and U proteins cannot yet be determined.