Biomedical subjects

K Munk

Publications and source records attributed to K Munk.

29 records · Page 2Linked to original sources

PubMed1977

Activation of an endogenous C-type RNA virus in rat embryo cells after transformation by herpes simplex virus types 1 and 2.

Reverse transcriptase activity was detected in the supernatants of rat embryo fibroblast cell cultures transformed by HSV types 1 and 2 at either the sub-optimal temperature of 20 degrees C or the supra-optimal temperature of 42 degrees C. Rat cells clones which had been transformed at 20 degrees C contained higher levels of C-type virus DNA polymerase than did cell clones which had been transformed at 42 degrees C. Syncytia formation typical for C-type RNA viruses occurred at passages higher than 24. The activation of endogenous C-type RNA viruses was independent of the virus and transformation method used.

Animals↗

PubMed1977

Protection against herpes simplex virus infection in mice by Corynebacterium parvum.

Corynebacterium parvum administered in mice prior to herpes simplex virus (HSV) infection significantly protected them against lethal encephalitis. This was seen both with a mouse strain highly susceptible to HSV and with one relatively resistant to HSV. Mice immunosuppressed by cyclophosphamide and showing an increased mortality after HSV infection were also protected by C. parvum pretreatment. However, C. parvum given simultaneously with or after HSV infection did not exert a therapeutic effect.

Animals↗

PubMed1977

Morphological transformation of rat embryonic fibroblasts by abortive herpes simplex virus infection: increased transformation rate correlated to a defective viral genotype.

Rat embryo fibroblasts were abortively infected with various stocks of herpes simplex virus type 1 strain ANG at 42 degrees. In uninfected controls all of the cells died during an 8-day incubation period at the elevated temperature, whereas varying numbers of cells in the infected cultures survived and formed colonies during subsequent incubation for 3--4 weeks at 37 degrees. All of the survivors appeared to be morphologically transformed. Two types of survivors, epithelial- and spindle-like cells, which occurred at a ratio of approximately 1:1 in all assays, could be distinguished. The observed survival rates increased from about 1 x 10-7 to 3 x 10-5, corresponding to increasing fractions (0--50%) of a defective genotype present in the infecting virus stocks. The individual survival rates do not depend exclusively on the quantity of defective virions. The existence of different subtypes of defective genomes as a further parameter is discussed.

Animals↗

PubMed1977

Scanning electron microscopic studies of herpes simplex virus transformed cells.

The surface morphology of herpes simplex virus transformed cells was examined by scanning electron microscopy in exponentially growing and density inhibited rat embryo fibroblast cultures. The cell surface of oncogenically-transformed cells became more villated and many microvilli showed branching. C-type virus particles budding from the cell surface were commonly observed. Virus induced cytopathic effects observed by scanning electron microscopy, included rounding up and detachment of degenerating cells from the substrate.

Cell Division↗

PubMed1976

Neoplastic transformation of rat embryo cells with herpes simplex virus.

Sprague Dawley rat embryo cells (REF) were transformed by inoculation with herpes simplex virus (HSV) and incubation at 42 degrees C for 8 days. The infected cultures were subsequently returned to 37 degrees C and two types of cell clone were isolated from foci of growing cells after 4 weeks. One of the clones consisted of epithelial-like cells and did not produce HSV (REF-Tep-NP). The second consisted of spindle-shaped cells and cultures of these cells persistently developed small areas of degeneration where production of infectious HSV (REF-Tsp-P) took place. An additional clone which did not produce any more HSV (REF-Tsp-NP) was isolated from REF-Tsp-P in the presence of HSV-antiserum. REF-Tsp-P and REF-Tsp-NP grew more rapidly than REF and also formed foci in soft agar. REF-Tep-NP had a growth rate between that of normal rat embryo cells and that of both REF-Tsp-NP and REF-Tsp-P and did not form foci in soft agar. REF-Tsp-NP cells, in contrast to REF-Tep-NP cells, were resistant to superinfection with HSV types 1 and 2. REF-Tsp-P and REF-Tsp-NP produced metastasizing sarcomas in rats. After inoculation of 10(3) REF-Tsp-NP cells into 1-day-old rats tumours developed rapidly. REF-Tep-NP cells did not induce tumours in rats. The parental REF cells produced no tumours, even when 10(8) cells were inoculated into the rats. Positive immunofluorescence was observed in all three transformed cells only with the hyperimmune rabbit sera but not with human anti-HSV reconvalescence immune sera.

Animals↗

PubMed1976

Replication of herpes simplex virus in mouse spleen cell cultures stimulated by lipopolysaccharide.

Replication of HSV was demonstrated in spleen cell cultures of D2 and several other strains of mice after prestimulation with mitogenic doses of LPS for 2 days. No viral replication occurred in unstimulated cultures or in cultures prestimulated with PHA and Con A, whereas there was some viral replication in spleen cell cultures of D2 mice after prestimulation with Poly I-C. Spleen cells of B6 mice did not support replication of HSV under any of the conditions we have tested thus far. The reasons for this defect are not clear, but it was obviously not caused by a defective lymphoproliferative response to LPS or by an active anti-viral principle elaborated by B6 spleen cells. F1 hybrids between B6 and D2 mice were capable of HSV replication to the same extent as were spleen cells of D2 mice. Several strains of both HSV-1 and HSV-2 could be replicated in D2 spleen cells cultures. Nylon column treatment of D2 spleen cells removed the ability to replicate HSV, whereas macrophage removal from the spleens by plastic adherence was without effect. Purified peritoneal exudate cells from D2 mice did not support replication of HSV. Together these data suggest that B cells activated by LPS represent the target cell of HSV replication in mouse spleen cell cultures.

Animals↗

PubMed1975