Florid CD4+, CD56+ T-cell infiltrate associated with Herpes simplex infection simulating nasal NK-/T-cell lymphoma. –

These observations are consistent with our working hypothesis that gE/gI can bind extracellular ligands, so-called gE/gI receptors that are concentrated at epithelial cell junctions. Get a printable copy (PDF file) of the complete article (581K), or click on a page image below to browse page by page. As an enveloped virus, HSV must fuse its membrane with a host membrane in order for replication to take place. These observations are consistent with our working hypothesis that gE/gI can bind extracellular ligands, so-called gE/gI receptors that are concentrated at epithelial cell junctions. Nuclear pores have diameters of 39-40 nanometers, whereas HSV-1’s diameter is about 120 nm, Wiggers explained. To this end, we inserted a ligand to HER2 in gD. The now cytosolic capsid then buds into a membranous organelle in the cytoplasm to obtain its final envelope.

This tethering is inadequate for proper cell spreading or movement to occur and may result in both excessive endothelial lift-off and impaired vascular repair in HSV infections. The G form of ICP0 was also absent in cells infected with R7914 mutant. A.), 1–604 (Academic, New York, 1972). To investigate whether HSV gB, gD, gH, and gL were sufficient to induce fusion, we expressed these glycoproteins under the adenovirus major late promoter of the Cos cell expression vector pSMH3. Such focusing on just a few key determinants provides a simple means for viruses to escape immune surveillance. Full text Full text is available as a scanned copy of the original print version. In comparison, 10 μM F3dThD-5′-PPP inhibited HEp-2 cell- and HSV-1-induced dTK 95 and 15%, respectively.


Analysis of the results suggest that prostaglandins can enhance cell-to-cell spread of HSV, but that cyclic AMP is probably not involved in this effect. None of these effects is seen following transfection with a control adenovirus that does not encode tk. In this report, we demonstrate that the partial block to HSV-1 infection in gro2C cells occurs in the virus entry pathway. This increased appearance of virus in liver tissue correlates with increases in cellular ribonucleotide reductase activity and DNA synthesis and is also associated with increased viral binding. The focus of this report is on the α22 gene. Get a printable copy (PDF file) of the complete article (637K), or click on a page image below to browse page by page. The interaction of gD with the cell surface was also inhibited by monoclonal antibody IV3.4., whereas other gD-specific monoclonal antibodies, despite their high neutralizing activity, were not able to inhibit this interaction.

The reviews here will highlight the general principles of herpes virus infection, with equal attention to overall principle and important difference. Full text Full text is available as a scanned copy of the original print version. Furthermore evidence was obtained that the mitochondria from liver tissue undergo a selective deterioration when infected with herpes virus. Confirming the reports of others, our results demonstrate that the CpG ODN-peptide approach generates an antigen-specific CD8+ T-cell population, but the frequency of CD8+ T cells is lower than that induced by VvgB(498-505). The major difference between the patients with herpes zoster and those without was the superior duration of median survival for the infected patients. The peripheral blood mononuclear cells were separated by Ficoll-Hypaque centrifugation. In addition, there was a suggestion that patients in long-term remission who had received primary combined modality therapy (radiotherapy plus chemotherapy) had an impaired response when compared to normal persons or to patients who had received single modality therapy.

Serological studies of the two related HSV serotypes (HSV-1 and HSV-2) have revealed both type-specific and cross-reactive antigenic determinants in the viral envelope and on the surface of infected cells. Replication of the herpes-type virus in the P3HR-1 Burkitt lymphoma cell line was studied. The virus-containing vesicle then traffics to the plasma membrane where it fuses, exposing a mature virion. A baby hamster kidney [BHK(tk-)] cell line (US11cl19) which stably expresses the US11 and alpha 4 genes of herpes simplex virus 1 strain F [HSV-1(F)] was found to be resistant to infection with HSV-1. Polyribosomes isolated from herpes simplex virus type I (HSV-1)-infected cells have been used to program a eucaryotic cell-free translation system. Intranuclear and intracytoplasmic virions of herpes zoster virus were easily and specifically identified due to intense staining by the finely granular, black reaction product. The target specificity of natural killer (NK) cells for either tumor cells or virus-infected cells has been investigated.

This article has been cited by other articles in PMC. Fifty-nine neonates with herpes simplex virus (HSV) infection were evaluated with use of assays for neutralizing antibody (NAb), lymphocyte transformation (LT), alpha interferon production, and virus-specific antibody (immunoblots). This article has been cited by other articles in PMC. * Final gross prices may vary according to local VAT. A rabbit T-cell line, BJ-610, has been derived from a New Zealand White rabbit infected with Alcelaphine herpes virus-1, which has the characteristics of a lymphokine activated killer (LAK) cell.