In addition to their physiological roles in cells, cdks are also involved in the replication of DNA-containing viruses. Thus, HSV replicates more efficiently in replicating than in growth-arrested cells. and S.E. and stained with DAPI or antibodies against Egr-1 or viral antigen glycoprotein D (gD). Selected References These references are in PubMed. ICP0 itself autoubiquitinates via its RING domain, a process counteracted by the ubiquitin-specific protease USP7, which is in turn subject to ICP0-mediated degradation (5, 10). It might also constitute one way to promote circularization of linear viral genomes containing extensive directly repeated sequences at the ends (7).

To address whether the cytoplasmic localization of ICP0 is a common feature of cells infected with all ICP4 mutant viruses or whether mutant ICP4 polypeptides, together with ICP27, determine the intracellular localization of ICP0, we used double-staining immunofluorescence tests to examine the intracellular staining patterns of ICP0 and ICP4 in cells infected with an extensive series of ICP4 mutant viruses. Get a printable copy (PDF file) of the complete article (4.2M), or click on a page image below to browse page by page. This may not be the complete list of references from this article. In contrast, activation in the TK hybrid cell types required viral gene expression and the presence of a functional IE175 gene product. Full text Full text is available as a scanned copy of the original print version. Get a printable copy (PDF file) of the complete article (1.8M), or click on a page image below to browse page by page. This may not be the complete list of references from this article.


Here we report a previously unknown function for ICP22 in the regulation of HSV-1 nuclear egress. Similar results were obtained upon infection of mouse epidermis with a keratinocyte-restricted deletion of the rac1 gene, indicating no inhibitory effect on HSV-1 infection in the absence of Rac1. Full text Full text is available as a scanned copy of the original print version. Here we report the development of highly disabled versions of HSV-1 deleted for ICP27, ICP4, and ICP34.5/open reading frame P and with an inactivating mutation in VP16. In Vero cells, 7134 was more sensitive to inhibition by low doses of type I IFN (-alpha/beta) or type II IFN (-gamma) than vesicular stomatitis virus, a well-studied IFN-sensitive virus. The potential regulation of the IE promoters by several different neuronally expressed POU proteins during the initiation, maintenance and re-activation of latent infection in sensory neurons is discussed. These 5′-terminal sequences were shown to be spliced to 3′-terminal cotranscripts of 1,450 bases (for IE mRNA-4) and 1,540 bases (for IE mRNA-5).

The synthesis of small amounts of Vmw 175 was specified by the 4.7-kb mRNA. However, temperature shift experiments in which tsLG4-infected cells were shifted to the nonpermissive temperature at various times after infection showed that the synthesis of late transcripts was not altered 2 hr after the shift whereas both the accumulation of leaky late and late mRNA and the incorporation of [35S]methionine into newly synthesized gB and gC was reduced by 2 hr after the shift to nonpermissive temperature. None of the patients had an underlying condition known to favour herpes zoster. These patterns of adsorption were found with all four HSV-1 and four HSV-2 strains tested. It was also noted that, at 9 h postinfection, under permissive conditions, VP175 was not found in association with nucleocapsids or enveloped particles. It was striking that HCF-1 was strictly required for VP16-mediated transcriptional induction via the core enhancer as well as for basal level transcription mediated by GA-binding protein and Sp1. This factor has been identified as a neuronal form of the octamer-binding transcription factor Oct-2, and this protein has been shown to be able to repress the IE promoter when Oct-2 is artifically expressed in normally permissive fibroblasts.

IFN did not prevent the HSV-1-induced early shut-off of host cellular protein synthesis caused by a structural protein of infecting virus. Additionally, we show that transient expression of ICP22 can trigger the loss of Ser-2P RNAP II in transfected cells. Five IE genes constitute the first set of genes to be transcribed upon HSV-1 infection. The results show that both reporter assays were sensitive to antiherpetic screening. Here we report that HSV-2, a close relative of HSV-1, is naturally resistant to LMB. HSV is a large virus, potentially allowing the insertion of multiple or very large transgenes. Here, we report that ICP0 interacts with SIAH-1, a cellular E3 ubiquitin ligase that is involved in multiple cellular pathways and is itself capable of mediating PML degradation.

The early events in herpes simplex virus infection were studied by means of radio-autography. The HSV-1 ‘immediate-early’ (IE) promoter sequences contain multiple copies of a hexanucleotide sequence, GGGCGG, known as a GC box, and one or more copies of an 11-base pair (bp) conserved A + T-rich element, designated TAATGARAT.