The herpes simplex virus type 1 (HSV-1) mutant 1814 possesses an insertion mutation that abolishes trans-activation of immediate early (IE) transcription by the virion protein Vmw65. Interactions between 1814 and the host cell were examined by use of an latency system which relies on infection of human foetal lung (HFL) cells at 42 °C to prevent lytic growth of virus. Mutant 1814 was retained in HFL cells after infection at low m.o.i. and incubation at 42 °C, and was reactivated by superinfection of monolayers with viruses that express the HSV-1 IE protein Vmw110. Moreover, latency was established by 1814 in an analogous manner at 37 °C. The low cytotoxicity of 1814 enabled an investigation of latency after infection at high m.o.i. (five particles per cell) to be undertaken. At 42 °C, or at 37 °C in the presence of an inhibitor of DNA synthesis, 1814 DNA was maintained at low abundance (one to eight copies per infected cell) in a non-linear configuration. The absence of trans-activation by Vmw65 therefore predisposes HSV to latency, as opposed to lytic growth, in HFL cells, resulting in the retention of the genome in a form resembling that found .


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