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This one the other hand can be the result of having oral sexual intercourse with the partner suffering from genital herpes. Therefore, cellular and viral membrane TGN proteins move to cell junctions at late times of HSV infection when the production of enveloped particles is blocked. The authors report that although apoptosis occurred rapidly in microglia, it was delayed during productive infection of astrocytes. Links to PubMed are also available for Selected References. In contrast to TGN membrane proteins, several cellular proteins that normally adhere to the cytoplasmic face of TGN, Golgi, and endosomal membranes remained primarily dispersed throughout the cytoplasm. Sciortino et al. Nectin-1 and gD colocalized at cell contact areas between infected and noninfected cells and at the edges of plaques.

Torrisi, Proc. These results suggest that the HLA D region-encoded class II antigens may be important in the recognition and destruction of virus-infected cells by human CTL. For example, ICP0 is sufficient to trigger HSV reactivation in latently infected trigeminal ganglion neurons [2], [3]. Tolerized mice were unable to generate protective cells. Other experiments have shown that HSV can activate the expression of endogenous type C retroviruses. Virol. These novel particles we term pre-viral DNA replication enveloped particles (PREPs).


In addition, our experiments suggest that these alternate sources are not available either in nondividing cells or in cells at 39.5 degrees. Although we found a slight increase of Rab27a expression after culturing cells under differentiation conditions, results obtained in both systems (DM versus GM) did not differ substantially. (ii) Soluble IL-13 but not IL-4 or IL-2 blocked the replication of R5111 recombinant virus in J-13R cells. Reports have indicated that HSV activates NF-kappaB during productive infection and this may be an essential aspect of its replication scheme [Patel, A., Hanson, J., McLean, T.I., Olgiate, J., Hilton, M., Miller, W.E., Bachenheimer, S.L., 1998. ICP0-deficient mutants are hypersensitive to IFN, as viral mRNAs do not accumulate in IFN-treated Vero cells whereas cellular mRNAs encoding IFN-induced gene products increase in abundance (10, 16, 17, 20). Moreover, a component compatible with a lipid-linked oligosaccharide present in DG treated cells was not observed in HSV infected TM treated cells. Us5 expression was delayed in the absence of ICP22; furthermore, expression of Us5 in trans protected cells from apoptosis induced by an HSV mutant with deletion of ICP27, suggesting that the antiapoptotic effects of ICP22 and ICP27 are mediated in part through effects on gJ expression.

Roizman, and M. We examined the ICP4 present in HSV-1 virions that were either derived from wild type infected cells or from ICP4-expressing (E5) cells infected with ICP4 deletion virus d120. In an effort to establish that phosphate turnover was occurring on the cellular dUTPase protein, cells were prelabeled with 32P-orthophosphate and then infected with HSV in the absence of label. Biol. The present data suggest that generalized viral infection due to cell-free viruses is fought mainly by CD4+ CTL, which have previously been reported to possess both cytotoxicity and helper function, and that localized viral infection on HLA class II-negative fibroblasts is prevented from spreading to adjacent cells mainly by CD8+ CTL. Furthermore, the blockade of NF-κB translocation by suppression of protein kinase R activation does not render the cell more susceptible to apoptosis induced by viral gene expression. The tubular structures appeared as early as 6 hours after infection and reached a maximum at 12 hours.

Several approaches were used to show that the cytotoxicity being detected was predominately of the direct type rather than antibody-dependent cell cytotoxicity (ADCC). Specific spectral biomarkers for rapid and reliable monitoring and identification of infected cells and probably for the discrimination between these viruses were searched. To characterize the molecular basis of the cell-virus interactions and to analyze the state of the latent HSV genome, an in vitro model system was established. Abstract: Herpes simplex virus (HSV) and Pseudorabies virus (PRV) are related herpesviruses that are important pathogens in their natural hosts. Cytochemical localization of the lysosomal enzymes acid phosphatase and arylsulfatase in cells infected by herpes simplex virus (HSV) or human cytomegalovirus (CMV) showed the following interactions between viruses and host cell lysosomes: (i) many enveloped progeny viruses were located within cytoplasmic vacuoles containing lysosomal enzyme activity; (ii) naked cytoplasmic capsids appeared to acquire an envelope by budding directly into lysosomes; and (iii) many of the cytoplasmic dense bodies that are characteristic of CMV-infected cells and are thought to represent noninfectious aggregates of CMV structural proteins (I. Recombinant baculoviruses were used to express the six capsid genes (UL18, UL19, UL26, UL26.5, UL35, and UL38) in insect cells. This article has been cited by other articles in PMC.

Herpes simplex virus 1 attaches to at least two cell surface receptors. Herpes simplex virus displays tropism for neurons and other polarized epithelial cells. Proc Natl Acad Sci U S A.