Search results for "Simplexvirus"
showing 10 items of 60 documents
Induction capacity and influence of dThdMP on thymidine kinase activity of type 1 and 2 strains of herpes simplex virus
1978
The thymidine kinase inducing ability of 104 strains of herpes simplex virus was studied comparatively. A pronounced relationship was established between induction of the enzyme and the serotype of the strains. As a rule, the strains of serotype 2 are weaker inducer of dThd- and dCyd-kinase activity than serotype 1 strains. A certain parallelism exists between induction of both enzymes, however the activity of the thymidine kinase increases after infection with herpes simplex virus 4--5 times more than that of the dCyd-kinase. Adaptation of the strains to cell cultures only slightly modifies the inducing ability of the herpes simplex virus strains. The thymidine kinase activity induced by H…
Ribonuclease H levels in herpes simplex virus-infected cells.
1980
Two forms of ribonuclease H (RNase H) have been identified both in uninfected and Herpes Simplex virus (HSV-)infected BHK cells. Identical RNase H species were detected in control- as well as in infected cells. RNase H I and II have not been found to be associated both with host cell DNA polymerase alpha and beta and HSV-induced DNA polymerase. Infection of BHK cells with HSV type 1 does not lead to a pronounced alteration of RNase H II activity but to an increase (3-fold) of the extractable RNase H I activity. RNase H I activity increases to a maximum between 8-10 hours p.i.; the bulk of HSV-DNA synthesis occurs between 6-8 hours p.i. From these experiments we draw the preliminary conclusi…
The region 0.7615-0.796 m.u. of the HSV-1 genome determines suppression of humoral antibody formation against herpes simplex virus.
1991
The influence of genetic properties of parts of the HSV-1 genome on suppression of humoral antibody formation was investigated by using intratypic recombinants. The deleted strain HFEM (HSV-1) induces suppression. The MluI DNA fragment (coordinates 0.7615–0.796 m.u.) derived from the antibody inducing strain F1 (HSV-1) was transfected into the deleted strain HFEM to produce the recombinant virus R-MlCI and shown to restore antibody formation, as demonstrated by neutralization- and ELISA-tests. The intratypic recombinant viruses R-15, R-19 and R-26, produced by transfection of the Bam HI DNA-fragment B (0.738–0.809 m.u.) of strain Fl into the deleted strain HFEM, resulted in antibody formati…
Die Hemmung der Riesenzellbildung durch das sogenannte Compound 48/80 nach der Infektion mit dem Herpesvirus hominis
1969
Es wurde uber die Wirkung des Histamin-Liberators Compound 48/80 auf die Phasen der Synthese des Herpesvirus hominis und auf normale Zellstoffwechselprozessein vitro berichtet.
Evidence for a multistep mechanism for cell-cell fusion by herpes simplex virus with mutations in the syn 3 locus using heparin derivatives during fu…
1994
Addition of heparin-Na+ as well as related substances of high and intermediate MW (Arteparon and polyanion SP54) 3 h after infection inhibit fusion from within (FFWI) induced by HSV strains with mutations in the syn 3 locus only. The concentration of heparin-Na+ required to inhibit FFWI is 10-fold higher (1 mg/ml) than that needed to inhibit adsorption. Instead of fusion, cell rounding is observed. The effect is readily reversible. A low MW heparin disaccharide is ineffective. Neomycin, at a concentration of 8 mM, inhibits FFWI induced by all HSV-1 but not HSV-2 strains, whereas adsorption is inhibited at 3 mM. We conclude from our observations that cell-cell fusion (FFWI) induced by syn 3 …
T-cell-mediated cytotoxicity against herpes simplex virus-infected target cells
1977
THE control of herpes simplex virus (HSV) infection by immunological mechanisms seems to be complex and is poorly understood. Neutralising antibodies to HSV plus complement seem to have no effect on the propagation of HSV infection, because HSV spreads to adjacent cells by passing through intercellular bridges1–3. Anti-HSV antibodies plus complement, however, destroy virus-infected cells, but cannot prevent the spread of HSV, suggesting that the virus must be transferred to neighbouring cells before immune lysis occurs1,5. Therefore if lymphocyte-mediated cytolytic mechanisms are instrumental in blocking the spread of HSV in vivo, they ought to destroy infected cells at a very early stage i…
Inhibition of giant cell formation by compound 48/80 after infection with herpesvirus hominis
1974
Choline kinase has been found to be a soluble enzyme with a molecular weight of 105,000 in the cytoplasm of primary rabbit kidney cells. It has been purified 150-fold. It was investigated whether the inhibiting effect of Cpd 48/80 on virus-induced giant cell formation is due to interference with this enzyme. Cpd 48/80-dimer was shown to inhibit the choline kinase activityin vitro without a concomitant inhibition of giant cell formation. Likewise, another competitive inhibitor of choline kinase, purinyl-6-histamine, does not prevent giant cell formation. This finding suggests that there is no correlation between choline kinase activity and giant cell formation.
Asymptomatic vaginal herpes simplex virus infections in mice: virology and pathohistology
1996
One of the causes of genital tract infections in humans are herpes simplex virus types 1 and 2 (HSV-1, HSV-2). Although primary and recurrent infections can be clinically apparent and in part very serious, many infections are asymptomatic and result only in temporary genital shedding of virus (recurrences). During our investigations of vaginitis, strain IES of HSV-1 produced an asymptomatic infection. Replication in the murine vaginal (vag.) epithelium as well as antibody formation after vag. infection was comparable to those of survivors after infection with highly virulent strains. Titration of liver, spleen, ovaries, adrenal glands spinal cord, or brain after vag. IES infection revealed …
Influence of double infections on the induction of thymidine kinase by UV-irradiated herpes simplex virus types 1 and 2 and pseudorabies virus
1975
Simultaneous infection of primary rabbit kidney cells with HSV type 1 TK+ and a TK- strain results in a mutual influence of both viruses on the induction of thymidine kinase (TK). TK+ virus has an enhancing and TK- virus a depressing effect on TK induction by a superinfecting TK+ virus. The enzyme induction depends on the ratio of multiplicities of both viruses. The mutual influence on TK induction depends further on the time of addition of the superinfecting virus: the effect of the second virus can still be observed when given 6 hours after primary infection. Identical phenomena can be observed using combinations with HSV type 2 or Pseudorabies viruses. The ability of HSV to induce TK is …
Relationship between HLA I surface expression and different cytopathic effects produced after herpes simplex virus infection in vitro.
1992
In the present study, we investigated the effects of herpes simplex virus (HSV) infection on the expression of HLA class I antigens and beta 2-microglobulin in human fibroblasts. The mRNA abundance for HLA class I was shown to be strongly reduced after infection with HSV strains either producing cell rounding or fusion from within (FFWI), however, HLA class I expression on the surface of cells is strongly reduced only after appearance of FFWI. Using a ts mutant (ts 78R) or CyA in combination with a fusion from without (FFWO) inducing strain of HSV, this loss of HLA class I antigens is assumed to be correlated to the rearrangement of the cell membrane during the fusion process itself as a la…