Role of glycoprotein B of herpes simplex virus type 1 in viral entry and cell

B-capsids do not contain viral DNA but instead contain the proteolytically processed forms of the internal scaffold (35, 50). It was also reported that PDTC could act as a specific inhibitor of the E3 ubiquitin ligase, targeting IκB for ubiquitination to influence proteasome-mediated IκB degradation (9). There is also an aberrant accumulation of primary enveloped virions in the perinuclear space and in the induced invagination structures in these cells (9–12). Movat’s pentachrome stain was also used in the study of plaque morphology. E-mail: Supporting the corneal autoantigen hypothesis is the observation that mice such as C57BL/6 (B6) and CB.17, which express the Ig2ab isotype and so are immunologically tolerant to the autoantigen, are highly resistant to HSK development (2, 21,35). We have previously reported changes at the INM after HSV infection, exemplified by altered diffusional mobility of the lamin B receptor; dissociation of a population of lamin A/C from the lamina (40); and hyperphosphorylation of a major nuclear membrane protein, emerin (29).

B capsids contain the internal scaffold proteins but no DNA, whereas A capsids are empty and are thought to result from abortive attempts at DNA encapsidation. The replication cycle of HSV begins with the initial attachment of virus to heparan sulfate (HS) moieties on the cell surface (34), which is mediated by glycoprotein C (gC) and gB (reviewed in reference 27). Inhibition of any of these stages blocks HSV-1 replication. These phenotypic changes facilitate migration of the DCs to the draining lymph nodes to initiate an antiviral T cell response. The repression of viral protein synthesis during latency has led to the prevalent view of latency as being a quiescent and antigenically silent infection that is ignored by host immunity. PKCs have been grouped into three structurally and functionally distinct subfamilies: conventional PKCs, novel PKCs, and atypical PKCs. These results suggest that transcriptional regulation of γ34.5 by cell cycle-regulated promoters can be used to target HSV-1 virulence toward tumors while maintaining the desirable neuroattenuated phenotype of a γ34.5 mutant.

Goals for microbicide development are that they be safe, affordable, stable, and active against multiple STIs. Such events are essential for downstream events, such as NF-κB activation and interleukin expression. Besides cytoplasmic roles in the activation of NFκB, recent studies have identified IKKα and the IKK scaffold protein IKKγ/NEMO in direct regulation of NFκB-dependent transcription in the nucleus (2, 49, 53). Links to PubMed are also available for Selected References. Links to PubMed are also available for Selected References. This finding brings the number of genes known to map in the unique short region of the herpes simplex virus type 1 DNA to 14 and the total number of different genes to 78. Similarly, cells transformed with the ICP4 gene of HSV-2 served as efficient hosts for the growth of d120, HSV-1 ICP4 deletion mutant.

Mutations in plasmids, including those located in the extracytoplasmic domain of gB, were identified that reduced the fusion activity of gB. There are two schools of thought about what happens next, one being that gD, after receptor binding, is able to bind to a preexisting complex of gB and gH/gL (6, 7) and the other being that gD, after receptor binding, is able to trigger the binding of gB to gH/gL (5). Approximately one third of the world’s population, more than 2 billion people, has the hepatitis B infection, including 350 million chronic carriers of the virus. These references are in PubMed. In conclusion, this is a previously undescribed mode of viral immune evasion involving hijacking of DR from its normal transport route to the cell surface, followed by viral-mediated release of DR into the exosome pathway. 1968; Heine et al. Links to PubMed are also available for Selected References.

DNA sequencing of this virus identified a single base reversion of the site II mar mutation, resulting in restoring of the wild-type sequence (Arg to Gly). This may not be the complete list of references from this article. In vitro translation of hybrid-selected mRNA indicated that among the proteins these mRNAs encode are an 82,000-dalton (d) polypeptide reactive with a monoclonal antibody against herpes simplex virus type 2 alkaline exonuclease and a 50,000-d polypeptide weakly reactive with a polyclonal antibody made against the capsid protein VP19C. Earlier studies have shown that the thymidine kinase-negative baby hamster kidney (BHKTK-) cell lines expressing constitutively the herpes simplex virus 1 (HSV-1) glycoprotein D (gD), designated BJ, restrict infection by HSV-1 at the level of virus entry. We report that US11/ beta-galactosidase fusion protein expressed in bacteria bound to rRNA from the 60S subunit and not the 40S subunit. N2 – Topical microbicides designed to prevent acquisition of sexually transmitted infections are urgently needed. The 773-residue ectodomain of the herpes simplex virus type 1 (HSV-1) glycoprotein B (gB) has been resistant to the use of mutagenic strategies because the majority of the induced mutations result in defective proteins.

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