Roizman, B., 1996, Herpesviridae, in: Fields Virology, 3rd ed., Volume 2 (B. Holland GN, Vaudaux JD, Jeng SM, Yu F, Goldenberg DT, Folz IC, Cumberland WG, McCannel CA, Helm CJ, Hardy WD; UCLA CMV Retinitis Study Group. When ICP0 is not synthesized, the HSV-1 genome is acutely susceptible to cellular repression. Rarely, HSV-1 reactivation can cause encephalitis; however, a third of the cases of HSV-1 encephalitis are associated with HSV-1 primary infection. However, we report here that HSV infection does not increase the rate of degradation of IEX-1 mRNA; rather, actinomycin D chase assays indicate that the transcript is stabilized relative to that in uninfected cells in both the presence and absence of functional vhs. Links to PubMed are also available for Selected References. The arrangement of the sequences encoding these proteins along the herpes simplex virus type 2 genome was determined by hybridization of the RNA to cloned PstI fragment of BglII-N and to single-stranded DNA segments cloned into M13mp7.
These are separated by two regions which have no effect on KOS activity, even though they contain 43 of the 74 amino acid differences between the parental alleles. In addition, alleles encoding a full-length KOS polypeptide with a 32-amino-acid N-terminal extension retain considerable activity. Hirsch, J. Infect Dis Obstet Gynecol. These results may also be clinically relevant. There is increasing evidence that HSV-1 and VZV latency is epigenetically regulated.