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Activation of herpes simplex virus (HSV) type 1 genome by temperature-sensitive mutants of HSV type 2
Journal article   Peer reviewed

Activation of herpes simplex virus (HSV) type 1 genome by temperature-sensitive mutants of HSV type 2

Brian L. Wigdahl, Harriet C. Isom, Erik De Clercq and FreD Rapp
Virology (New York, N.Y.), v 116(2), pp 468-479
1982
PMID: 6278723

Abstract

Previous studies have demonstrated that herpes simplex viruses (HSV) type 1 (HSV1) and type 2 (HSV-2) can be maintained in a repressed form in human embryo lung cells. Reducing the incubation temperature or superinfecting with a heterologous herpesvirus, human cytomegalovirus (HCMV), results in activation of virus replication. We now report that superinfection with a partially homologous herpesvirus, HSV-2, also resulted in activation of HSV-1. To minimize excessive synthesis of infectious HSV-2 while allowing virus gene expression, repressed HSV-1-infected cultures were superinfected with HSV-2 temperature-sensitive (ts) mutants ( tsF3, tsB5, or tsH9). The predominant virus replicated after HSV-2 is mutant superinfection at a nonpermissive temperature was identified as activated parental-like HSV-1 by (i) plaquing efficiency at permissive (34°) and nonpermissive (40.5°) temperatures, (ii) sensitivity to inhibition by the HSV-1-specific antiviral agent (E)-5-(2-bromovinyl)-2′-deoxyuridine, and (iii) restriction endonuclease cleavage analysis. In addition, the fact that superinfection with HSV-2 tsB5 or tsH9, which are unable to synthesize virus DNA and express only early virus genes at nonpermissive temperature, resulted in synthesis of virus demonstrated that HSV-2 DNA synthesis is not required for activation. This system has provided the basis for further studies concerning the regulation of HSV gene expression in human cells.

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Virology
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