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Mammalian ribonucleotide reductase is a complex enzyme modified in its activity by a complex regulatory system involving adenosine triphosphate (ATP) and deoxyribonucleoside triphosphates. Infection of KB cells with herpes simplex virus (HSV) type 1 or 2 induces the formation of an altered ribonucleotide reductase. The properties of partially purified reductase from uninfected KB cells have been compared with the enzymes obtained from HSV-1 and HSV-2 infected KB cells. We found that the virus-induced enzymes are similar to the KB enzyme in some properties but differed significantly from the host enzyme in three respects: (1) virus induced reductase was not inhibited significantly by deoxythymidine triphosphate regardless of ATP concentration, (2) magnesium was not required for virus enzyme activity although 2 mM-Mg2+ did stimulate the reaction, and (3) magnesium concentration required for optimal activity was different for virus and host enzymes. These changes are evidence that the enzyme molecules present after infection by HSV-1 or HSV-2 differ from those present before infection.
J Gen Virol 1977 Jul
PMID:Ribonucleotide reductase from herpes simplex virus (types 1 and 2) infected and uninfected KB cells: properties of the partially purified enzymes. 1 50

Cytoplasmic vacuoles induced during transformation of cells by Bryan strain Rous sarcoma virus (RSV-BH) have been studied using the cationic dye, neutral red(NR). Both the rate of uptake and the accumulation of NR are greater in RSV-BH transformed cells than non-transformed cells however, uptake was greater in vacuolated than in non-vacuolated cells, whether or not they were transformed. The NR was incorporated into pre-existing vacuoles in the absence of cytoplasmic staining, suggesting the existence of direct channels from the cell surface to the vacuoles. Other low mol. wt. cationic dyes could also be incorporated into vacuoles, although those with branched structures or cationic weights greater than 330 were excluded. No anionic dyes were incorporated. Infection of cells with a virus mutant, RSV-BH-Ta, induces temperature-dependent vacuolization. After a shift to the vacuole-permissive temperature, vacuoles developed at different rates and with morphological variations with different cations. Vacuoles which had formed in the presence of several cations, (K+, Rb+, tris+, choline+) failed to disappear when cells were incubated at a temperature sufficient to revert vacuoles formed in Na+-containing medium. No short-term effects of Cl-replacements (Br-, I-, or SO2-4) on vacuolization or reversal were observed. The results suggest that these vacuoles are organelles involved in cation uptake. A possible function for these organelles in RSV-BH induced malignancy is discussed.
J Gen Virol 1978 Mar
PMID:Cytoplasmic vacuoles of Rous virus transformed cells are organelles involved in cation uptake. 2 77

Minicells produced by B. subtilis CU403divIVB1 and infected by SPP1 synthesize at least 46 polypeptides which can be separated by polyacrylamide gel electrophoresis. These polypeptides represent the expression of 86% of the SPP1 genome's coding capacity. Infection of minicells by sus mutants and deletion mutants of SPP1 has permitted a correlation of genetic location with gene product and has shown that SPP1 normally synthesizes at least 8 non-essential polypeptides. Restriction fragments of SPP1 produced by EcoRI digestion of SPP1 DNA have been purified and used as template DNA in a coupled transcription/translation system derived from E. coli to determine the polypeptides encoded by the individual fragments. SPP1 expression in minicells differs from SPP1 expression in nucleated cells (Esche, 1975) in that late syntheses are not dependent on phage DNA replication in infected minicells.
Mol Gen Genet 1979
PMID:Bacteriophage SPP1 polypeptides synthesized in infected minicells and in vitro. 4 10

Infection of Bacillus subtilis 168Wt by SF 6 resulted in a rapid reduction in the number of phages. This could be counteracted by the addition of calcium, barium or strontium ions. At the optimum concentration of 7.5 x 10(-2) M, the number of p.f.u. remained constant until lysis began. Although cultures of another host. B. subtilis 31 try- his-, at the end of the logarithmic growth phase produced a substance which inactivated free phages, this was not the major cause of the reduction in the numbers of p.f.u. during infection experiments at low Ca2+ concentrations. The diminution of the number of p.f.u. was therefore attributed to the fact that at least one of the steps of the lytic cycle was calcium dependent. Adsorption of SF 6 was equally effective in media containing high or low concentrations of calcium ions. Infection experiments with phages whose DNA had been labelled radioactively revealed that, at high concentrations of calcium ions, the label remained associated with the host cells until lysis commenced. At low concentrations, however, a dissociation between phage DNA and the host was found, although adsorption took place at a normal rate. From these experiments we concluded that a high concentration of calcium ions was required for the penetration of phage DNA. Similar experiments with phages whose protein coat had been labelled showed the same results, indicating that desorption of the inactivated phages occurred. Both electron microscopy and column chromatogarphy with hydroxyapatite showed that a considerable fraction of the inactivated phages had ejected their DNA into the medium. A hypothesis explaining these results is presented.
J Gen Virol 1979 Feb
PMID:Effect of calcium ions on the infection of Bacillus subtilis by bacteriophage SF 6. 10 92

Human cells derived from both normal and neoplastic tissues can be infected by Mason-Pfizer monkey virus (MPMV) without accompanying cytopathology. Infection of cell cultures such as human rhabdomyosarcoma (A204) results in a persistenly infected cell line which can be subcultured over 30 sequential culture passages without significant change in phenotype properties according to reverse, transcriptase (RT), MPMV p27 antigen content, virus particle count and infectivity titre. Productive virus infections were established at relatively low virus particle (VP) input multiplicities (p.i.m.; about 0.06 VP/cell) In A204 cell cultures. At higher p.i.m. (about 600 to 6000 VP/cell) newly synthesized virus was detected within 4 days post infection. Although virus production was cumulative following primary infection, after subculture of infected cultures MPVM production was greater during active cell division. Using synchronization techniques, MPMV replication in persistently infected cultures was found to be cell cycle-dependent. The major internal antigen, p27, was synthesized in G2 and newly synthesized virus particles were released predominantly during mitosis and early G1. Colcemid arrest of cells during mitosis inhibited subsequent MPMV release. Consequently, production of extracellular virus depends upon the progression of cells through the mitotic stage. These data, which provided a basic understanding of the virus-host relationship that occurs in primate cells productively infected with MPMV, were used as a guideline for isolating MPMV-like viruses from experimentally and naturally infected Rhesus monkey.
J Gen Virol 1979 Aug
PMID:Characterization of infection and replication of Mason-Pfizer monkey virus in human cell cultures. 11 35

A group of RNA viruses, echovirus, poliovirus, reovirus, respiratory syncytial virus and Semliki Forest virus have been examined for ability to grow in enucleate African green monkey kidney (BSCi) cells. Semliki Forest virus produced an almost normal yield of virus but poliovirus, echovirus, reovirus and respiratory syncytial virus, although showing clear evidence of virus replication when compared with a nuclear DNA virus (pseudorabies virus) gave much lower yields than those from nucleate cells. Analysis of enucleate cells infected with echovirus and reovirus showed no evidence of a specific block in the synthesis of any virus-specified polypeptide. Infection with vesicular stomatitis virus at intervals after enucleation demonstrated a diminishing ability to support virus growth with increasing time. It is suggested that the yield of virus obtained from an enucleate cell is related to the length of the growth cycle of the virus, the reduced yield obtained with some viruses reflecting the declining ability of the enucleate cell to support virus growth.
J Gen Virol 1975 Feb
PMID:Virus development in enucleate cells: echovirus, poliovirus, pseudorabies virus, reovirus, respiratory syncytial virus and Semliki Forest virus. 16 89

Infection of human embryonic fibroblast cell monolayers with neutral red and light-inactivated herpes simplex virus, type 2 (HSV-2) at supra-optimal temperature (42 degrees C) resulted in persistence of viable cells in suspension culture at 37 degrees C which have properties in common with virus transformed cells: formation of cell aggregates, HSV-2-specific antigens and colony formation in soft methyl cellulose medium. These data are consistent with the idea that photodynamic inactivated HSV-2 has potential oncogenic activity.
J Gen Virol 1976 Feb
PMID:Transformation of human embryonic fibroblasts by photodynamically inactivated herpes simplex virus, type 2 at supra-optimal temperature. 18 35

Infection of mouse L cells with VSV leads to the formation of polykaryocytes about 4 to 12 h p.i. When anti-VSV immune serum was added during the course of infection, progression of cell fusion was soon suppressed. Cycloheximide completely suppressed the cell fusion when the drug was added within 1 h p.i., while the cell fusion was not suppressed at all when the drug was added at and after 3 h. Early polykaryocyte formation, 'fusion from without', was observed only at a low level in cells infected at very high multiplicities. The development of cell fusion induced by VSV was found to be different in several cell types, although all these cells produced a rather high yield of virus: L and C-243-3 mouse cell lines showed a high level of polykaryocytosis (80 to 100%), BHK and RK-13 cells responded at low level, and PS and Vero cells showed no cell fusion in response to VSV infection. In PS cells, however, cell fusion occurred when VSV-infected L cells were co-cultivated. From these observations, the mechanism of cell fusion induced by VSV was discussed.
J Gen Virol 1976 Jul
PMID:Polykaryocyte formation induced by VSV in mouse L cells. 18 16

Infection of interferon-treated L cells with VSV led frequently to the establishment of L cells persistently infected with VSV (LVSV cells). These cells were characterized by the following properties; (I) no supplement of antiviral factors such as anti-VSV antiserum, interferon, was required for their maintenance; (2) virus antigens were detected in about 5 to 30% of the cells by immunofluorescence staining; (3) the cells were not only resistant to superinfection by homologous virus, but also resistant to challenge by heterologous viruses such as Mengo virus; (4) the cells were destroyed by co-cultivation with heterologous cells susceptible to VSV infection; (5) the cells could be cured by serial cultivation in medium containing antiviral antibody, and the cured cells were as susceptible to VSV as normal L cells. It was shown that at least three factors (interferon, defective interfering [DI] particles and a selection of small-plaque temperature-sensitive [ts] mutants) took part in the maintenance of LVSV cells although it was difficult to evaluate exactly the relative importance of these factors. The effect of antiviral antibody, interferon and incubation temperature upon the maintenance of LVSV cells are discussed further.
J Gen Virol 1977 May
PMID:Studies of L cells persistently infected with VSV: factors involved in the regulation of persistent infection. 19 7

Infection with herpes simplex viruses type 1 or 2 prevented the aggregation of 7-day-old chick heart cells into smooth, spheroidal, spontaneously beating aggregates. Virus infection also caused a loosening of peripheral cells in aggregates formed from initially uninfected cells. Measurements of rate of attachment of labelled single heart cells to a monolayer of like cells (homotypic), to HEp-2 cells (heterotypic), or to plastic substrata (nonspecific adhesion) indicated that virus infection caused a significant but differential loss of homotypic and nonspecific adhesiveness, but no alteration in heterotypic attachment rates. These observations indicate that those cells surface changes induced by viruses which are related to cell adhesion can be quantified by techniques measuring attachment rates.
J Gen Virol 1978 Mar
PMID:Reduction of intercellular adhesiveness of chick heart cells by herpes simplex viruses 1 and 2. 20 31


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