This may not be the complete list of references from this article. The absence of any of these proteins abolishes the entry process. In vivo, HSV resides primarily in epithelial and neuronal tissues and spreads rapidly and efficiently, often in a directed fashion, between cells. The second article, published in December, describes the NEC’s crystal structure, knowledge of which is fundamental to the development of inhibitors. To engineer R-LM113, we removed a large portion at the N-terminus of gD (from aa 6 to aa 38) and inserted scHER2 sequence plus 9-aa serine-glycine flexible linker at position 39. Other models of virion egress propose that nucleocapsids can exit the nucleus through an expanded nuclear pore (33, 34), or that the original virion envelope derived from the inner nuclear membrane is retained throughout egress (13). In contrast, the activity of cdk2 exhibited by immunoprecipitated protein was reduced and resistant to roscovitine and may represent a contaminating kinase activity.
by Kurstak, E. Ligation of the gB coding region from pING14.2gB (nucleotides 52765 to 56099) (1) into theEcoRI site of pSMH3 generated pSMH3gB, while gD coding sequences (nucleotides 138345 to 139762) derived from pRVF6 (21) were excised as aHindIII-NruI fragment and ligated between theHindIII and EcoRV sites of pSMH3 to generate pSMH3gD. Alternatively, this immunodominance can potentially provide advantages to the infected individual, such as the ability to mount a rapid and high-affinity response while minimizing the possibility of cross-reactivity with self components (20). These references are in PubMed. Get a printable copy (PDF file) of the complete article (917K), or click on a page image below to browse page by page. Moreover, although the number of HSV-1 plaques that formed in gro2C monolayers was reduced by 85%, the plaque morphology was normal, and the virus released from the mutant cells was infectious. In conclusion, the early stages of hepatic regeneration after resection provide an environment suitable for viral replication.
A smaller transcript originating in the domain of the gene, designated US1.5, directs the synthesis of a protein containing the carboxyl-terminal 273 amino acids of ICP22 (8). This may not be the complete list of references from this article. Get a printable copy (PDF file) of the complete article (1.7M), or click on a page image below to browse page by page. These references are in PubMed. Selected References These references are in PubMed. Still, our results indicate that the CpG ODN-peptide immunization system holds promise as a means of selectively inducing a CD8+ T-cell response against HSV. As more effective and intensive chemotherapy prolongs the survival of patients with solid tumors, it is possible that the frequency of herpes zoster infection may approach that observed in patients with lymphoproliferative malignancies.
Baseline natural killer cell values (mean +/- SE) for pregnant patients (13.4% +/- 2.4%) and nonpregnant patients (19.8% +/- 3.7%) were similar. In two patients herpes zoster developed after the demonstration of absent in vitro lymphocyte reactivity to the VZ antigen. CTL generated by restimulation with the heterologous virus were capable of recognizing only the cross-reactive determinants on either HSV-1- or HSV-2-infected target cells. An apparent growth curve of the virus was constructed. The examination of infected Vero cells by electron, confocal, and total internal reflection fluorescence (TIRF) microscopy revealed that HSV-1 was released at specific pocket-like areas of the plasma membrane that were found along the substrate-adherent surface and cell-cell-adherent contacts. An escape mutant of HSV-1(F), designated R5000, that forms plaques on US11cl19 cells was selected. HSV-specific polypeptides synthesized in vitro are precipitated with antiserum to HSV-infected cell proteins.
Advantages of this technique over the ferritin-labeled antibody method include simpler preparative procedures for reagents, greater penetrability of the antibody conjugate, and internal amplification which substantially improves the ability to localize sites of antigen-antibody reaction. Both NK-sensitive (K562 cells) and NK-resistant (Raji cells) targets were lysed by three cloned lines of NK cells. With simian virus 40, intranuclear virions were not stained, whereas intracytoplasmic particles appeared densely black. Infants with encephalitis showed a broader spectrum of IgG and IgM antibody reactivity against HSV proteins by immunoblotting than did those who had earlier onset of mucocutaneous illness. Vero cells, HeLa cells, and pig kidney (MVPK) cells that produce gp50 all gave reduced yields of PRV and HSV progeny viruses when compared with the parent cell line or the same cell line transfected to produce a different protein. A genetically modified cell culture with a virus-inducible marker is described here, using a frequently isolated DNA virus (herpes simplex virus) as a model. Three antigens are expressed on BJ-610 but not RL-5.
The optimized three-layer indirect immunogold-labeled cryosection electron microscopy described is recommended for studies of virus-cell interactions, because: (1) it is a simple and reproducible method; (2) colloidal gold markers are electron-dense, stable, and easy to recognize; (3) the membraneous ultrastructure and immunolabeling are well preserved; (4) immunolabeling is less in the two-layer method; (5) silver-enhanced gold particles vary in size and shape; (6) it is possible to demonstrate herpes simplex virus type 1 glycoproteins gC-1 and gD-1 in the nuclear membranes and gC-1- and gD-1-labeled viral particles in the perinuclear space and to observe virions in the endoplasmic reticulum and Golgi area.