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At least 1,639 records · Page 91Linked to original sources
PubMed1976

Analysis of baby hamster kidney cells persistently infected with lymphocytic choriomeningitis virus.

Baby hamster kidney cells were persistently infected with lymphocytic choriomeningitis (LCM) virus (BHKpi cells). After 21 passages of the BHKpi cells infectious virus could no longer be detected; however, the cultures continued to produce LCM virus particles which interfered with the replication of infectious LCM virus in BHKpi cells and protected mice from a subsequent intracranial inoculation of infectious LCM virus. Cultures of BHKpi cells appeared to consist of three cell populations: uninfected cells, infected cells containing infectious LCM virus, and infected cells releasing interfering particles of LCM virus.

Animals↗
PubMed1977

The uncoupled relationship between the temperature-sensitivity and neurovirulence in mice of mutants of vesicular stomatitis virus.

Inoculation of wild-type (wt) VSV intracerebrally (i.c.) in Swiss weanling mice results in a rapidly fatal illness with death in two to three days. In contrast, i.c. inoculation of temperature-sensitive (ts) VSV mutants G3I and G22, but not ts GII or ts G4I, results in a more slowly progressive central nervous system (CNS) disease with distinct neurological signs. Studies undertaken to evaluate the neurovirulence of ts VSV mutants indicated that the ability of ts mutants to produce pathological changes in the CNS of mice appeared related to their ability to replicate to high titre in brain and spinal cord. However, replication of ts VSV mutants in brain alone was not sufficient to produce clinical illness. More importantly, the ability of ts VSV mutants to replicate at non-permissive temperatures in vitro did not appear to correlate with neurovirulence. VSV harvests from brains and spinal cords of mice infected with each of the ts mutants were temperature-insensitive. In spite of their temperature-insensitivity, the biological behaviour of viruses recovered from CNS tissues was, surprisingly, not that which was characteristic of revertant clones. Virus isolates recovered from infected CNS tissues, despite their temperature-insensitivity, behaved biologically like the orignal stocks of ts mutant virus. These data suggest that temperature-sensitivity is not directly correlated with the unique pathogenesis elicited by infection with ts VSV mutants.

Animals↗
PubMed1977

Studies of L cells persistently infected with VSV: factors involved in the regulation of persistent infection.

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.

Animals↗
PubMed1977

A study of events in chick cells infected with human adenovirus type 5 and their relationship to the induction of interferon.

In an attempt to define the molecular events involved in induction of interferon, various parameters of chick cells infected with human adenovirus type 5 were analysed. It was shown by digestion with various proteolytic enzymes and by disruption of the purified virus that induction of interferon requires the interaction of infectious virus with the chick cells. Analysis of adenovirus-infected chick cells by immunological and biochemical techniques indicated that most of the cells produce some virus-specific components, and that temperature sensitive mutants which fail to induce interferon at the restrictive temperature fail to synthesize late components at that temperature. However, since it has been shown that interferon can be induced in the absence of DNA synthesis, these studies conclude that interferon induction results from an early interaction between virus (or virus product) and chick cells and moreover that this interaction is also necessary for the synthesis of virus DNA in this system.

Adenoviruses, Human↗
PubMed1978

Characterization of snap-back RNAs in vesicular stomatitis defective interfering virus particles.

VSV defective interfering particles of various sizes and from several independent sources frequently contain plus and minus strand RNA. In many cases some of the complementary strands are covalently linked as snap-back molecules. Infectious particles on the other hand package little or no plus strands. Snap-back molecules from the three different sources examined so far vary in size but appear to conform to the same overall linear duplex structure with cross-links at the ends only. They each contain a base sequence which is a subset of the next larger one and appear to correspond to unique sequences in the L cistron of the genome. Possible origins for these snap-back molecules are discussed.

Defective Viruses↗
PubMed1978

Inverted complementary terminal sequences in single-stranded RNAs and snap-back RNAs from vesicular stomatitis defective interfering particles.

Complementary single-stranded RNAs from three independent VSV defective interfering particle (DI) sources examined can anneal and give rise to monomeric and multimeric circular and linear double-stranded structures observable by electron microscopy under aqueous conditions. When the RNA from the shortest of these DI is spread from 80% formamide solutions, as many as 32% of the molecules are circular, suggesting that the single-stranded RNAs contain inverted complementary terminal sequences. This is strongly supported by the isolation of the putative terminal sequences which rapidly become RNase resistant base-paired structures after melting and quick-cooling the RNA. RNase digestion yields a major and a minor component, 60 to 70 and 135 to 170 nucleotides long respectively. Snap-back DI RNAs also contain inverted complementary sequences at both ends of the plus and minus strands of the duplexes since nicking these at the ends gives rise to double-stranded molecules which can form monomeric and multimeric circular and linear molecules. Thus, snap-back molecules most likely contain a covalent linkage between or near complementary terminal sequences on the two complementary strands as schematically shown in Fig. 5D.

Base Sequence↗
PubMed1978

Prevention of death in Semliki Forest virus-infected mice by administration of defective-interfering Semliki Forest virus.

Adult mice inoculated with Semliki Forest virus (SFV) were protected from a lethal infection of the central nervous system by intranasal administration of defective-interfering (DI) SFV. DI SFV was prepared by eight passages at high m.o.i. in BHK 21 cells. Mice were treated with unpurified, unconcentrated tissue culture fluid which had been u.v.-irradiated to inactivate the infective virus present. Prevention of death was maximal when the DI virus was administered simultaneously with the infecting inoculum, and under the same conditions multiplication of infective virus in the brains of treated mice was reduced by 10(5)-fold. It was shown that DI SFV was propagated in mouse brains followed intranasal inoculation and it was concluded that protection was brought about through the intrinsic interfering capacity of the DI virus.

Animals↗
PubMed1978

Simultaneous production of mouse endogenous virus and Rous sarcoma virus by Schmidt-Ruppin virus infected mouse cells.

Schmidt-Ruppin Rous sarcoma virus infected chick cells injected into newborn C3H/f mice gave rise to tumours at the site of inoculation. These tumours were transplantable in adult C3H/f mice and were able to induce tumours in the wing of adult Leghorn chickens. Tumour cells from the 18th passage in mice were used to establish a cell line in tissue culture (C3HSR). These cells released C-type virus particles that produced foci and were able to propagate in chick cells. Cloning of the C3HSR cells demonstrated that the same cell expressed both avian and murine antigens. Mouse cells infected with virus released by C3HSR cells produced murine leukaemia virus-like particles as revealed by the reverse XC syncytial test and by immunofluorescence tests.

Animals↗
PubMed1978

Excess of interfering over infectious particles in herpes simplex virus passaged at high m.o.i. and their effect on single-cell survival.

The capacity of herpes simplex virus to kill cells and to form both infectious centres and progeny virus was studied in cell culture. Two virus stocks were compared at various m.o.i.: (i) a standard virus stock and (ii) a stock which contained interfering virus particles (I particles). The formation of infectious progeny virus as well as of infectious centres appeared to be reduced by the action of I particles. In the examined virus stock I particles exceeded infectious particles by at least a factor of 5 to 10. More than 50% of cells which could be demonstrated to be hit by I particles survived and formed colonies.

Cell Line↗
PubMed1979

Determinants of spontaneous recovery and persistance in MDCK cells infected with lymphocytic choriomeningitis virus.

MDCK cells that normally would have been killed by standard lymphocytic choriomeningitis (LCM) virus were saved either by pre- or co-infection with defective interfering (DI) virus. The ability of these spared cells to produce virus-specific antigen (as well as infectious virus) and resist being killed by standard virus challenge was followed for at least 35 days. During this period both types of cultures displayed unique cycling patterns for the above characteristics. The most striking difference was the longevity of the infections. Cultures exposed to DI particles prior to standard virus became persistently infected, while co-infection with both virus types led to spontaneous curing with no trace of the previous infection. The basis for these dissimilar outcomes was traced to a hitherto undetected non-defective LCM virus (called SP) in the DI virus stocks used to preinfect MDCK cells. SP virus was not present in standard virus stocks but arose in long-term persistently infected L cells that had been initially infected with standard virus. Cloned SP virus shared species-specific antigens with standard virus, was resistant to inhibition by DI virus and was capable of turning self-curing cultures into cultures persistently synthesizing both DI and SP virus.

Animals↗
PubMed1979

Evidence for herpes simplex virus type-selective receptors on cellular plasma membranes.

Herpes simplex virus type 1 (HSV-1) interfered with the adsorption of subsequently added homotypic but no heterotypic HSV, suggesting that the cellular receptors involved were type-selective. Both infective and u.v.-irradiated virus could block the attachment of virions to cellular surface receptors. The adsorption rate was studied by assaying non-adsorbed infective virus remaining in the fluid medium and cell-associated 3H-thymidine labelled HSV, and HSV mutants assayed in presence of phosphonoformic acid (PFA). The adsorption profiles indicated that GMK AH-1, Vero and SIRC cells all exhibited more HSV type 1-than type 2-selective receptors while HeLa S3 cells displayed more receptors with affinity for type 2 than for type 1. On HEp-2 and human embryonic lung cells HSV type 1- and type 2-selective receptors were about equally represented.

Adsorption↗
PubMed1979

Modulation by cell trypsinization of Sendai virus expression in African green monkey kidney cells: first infection and establishment of a carrier state.

Two African green monkey kidney (AGMK) cell lines, 37RC (interferon-producing) and Vero (non-interferon-producing), were infected by egg-grown Sendai virus passaged in eggs at high and low m.o.i. The appearance of haem-adsorption, and cytopathic effect (c.p.e.) as well as the presence of haemagglutinating virions in the supernates were much more pronounced with a virus seed obtained with 10(-3) diluted passages than with a seed obtained with undiluted inoculum. They were also independent of interferon production (data obtained in 37RC and Vero cells were almost superimposable). In studies carried out with the virus seed prepared at high dilution the establishment of infection was maximal when monolayers were infected as soon as 5 h after trypsinization and cell seeding, regardless of cell density. Virus in supernates obtained from cultures infected 5, 20 or 50 h after seeding exhibited a greatly reduced infectivity for monkey cells, but not apparently for chick embryos. Trypsin treatment of the virus supernates restored their infectivity for AGMK cells more efficiently for virus released from cells infected 5 h after seeding than for virus released from cells infected later after seeding. In keeping with these observations, virus in supernates from cultures infected 5, 20 or 50 h after seeding contained increasing amounts of auto-interfering virions. The decreased infectivity obtained in cell supernates was not accounted for by major differences in virus RNA synthesis. Similarly, the optimum infection established in cells seeded only for 5 h was not due to increased virus adsorption. Several lines of cells surviving first infection with egg-grown Sendai virus have been obtained and kept in cultures for 3 to 18 months. Virus release and c.p.e. apparently become reduced in the cells surviving the first infection until the newly repopulated monolayers must undergo trypsinization. Weekly protease treatments of the cells reactivate all parameters of virus infection which again will tend to disappear slowly and then reappear following each trypsinization ('intermittent' carrier state). The establishment and the 'intermittent' reactivation of these lines were not prevented by the inclusion in the medium of anti-Sendai virus serum. Temperature-sensitive ts functions do not seem to play an important role in this virus-host relationship.

Adsorption↗
PubMed1980

A sensitive method for quantification of vesicular stomatitis virus defective interfering particles: focus forming assay.

A focus-forming assay for the quantification of defective interfering (DI) particles of vesicular stomatitis virus (VSV) is described. This assay is based on the procedures described for lymphocytic choriomeningitis (LCM) virus by Popescu et al. (1976). Under appropriate conditions this focus-forming assay can quantify fewer than 100 DI particles/ml in a preparation containing a large number of infectious particles.

Animals↗
PubMed1980

Requirements for DI particle prophylaxis against vesicular stomatitis virus infection in vivo.

In contrast to biologically active DI particles, neither u.v.-inactivated standard virus nor either of two different homologous u.v.-inactivated DI particles showed any prophylactic effect when injected intracerebrally into mice concomitantly challenged with VSV. Although u.v.-inactivated DI particles did not prevent death when given with the challenge virus, they did significantly lengthen the time until death occurred. Also, both u.v.-inactivated standard virus and DI particles protected mice against late challenge (at 3 or 10 days after treatment). Dosage titrations of preparations of two different active DI particles showed significant prophylaxis against simultaneous challenge with numbers of DI particles 10- to 100-fold lower than those which gave no prophylaxis when u.v.-inactivated. Thus, prophylaxis in this system in this system required biologically active DI particles.

Animals↗