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At least 415 records · Page 23Linked to original sources
PubMed1983

Characterization of a non-syncytiogenic autonomously replicating variant of measles virus.

A variant, derived from both measles and subacute sclerosing panencephalitis virus preparations, incapable of producing intercellular fusion or syncytia typical of measles virus infections is described. This non-syncytiogenic (N-S) virus was easily detected using immunofluorescence, was genetically stable and replicated autonomously. The variant was defective in the production of both infectious virus and haemagglutinin in Vero and Hep2 cells. Persistent infections in Hep2 cells were readily established without the cooperation of defective interfering particles or temperature-sensitive mutants, although interferon could be detected. It is possible that such N-S variants may be involved with the regulation of persistent infections by measles virus.

Animals↗
PubMed1984

Monoclonal antibodies to the S1 spike and membrane proteins of avian infectious bronchitis coronavirus strain Massachusetts M41.

We have established four murine hybridoma cell lines which secrete specific antibody to avian infectious bronchitis virus (IBV) strain Massachusetts M41. Two monoclonal antibodies reacted with the spike protein and two reacted with the membrane protein. The specificity of the monoclonal antibodies for the external structural proteins was detected by immunoprecipitations using radiolabelled virus. The reactions of the monoclonal antibodies showed that one (S1) of the two glycopolypeptides associated with the spike protein has a strain-specific region involved in neutralization and haemagglutination, and the membrane protein has antigenic determinants which are present on the three strains of IBV tested (M41, Beaudette and D41).

Antibodies, Monoclonal↗
PubMed1984

Establishment and maintenance of persistent infection by the Phlebovirus Toscana in Vero cells.

Persistent infections were established by serial undiluted passages of the Toscana virus of the genus Phlebovirus in Vero cells. Persistence was maintained through more than 70 passages over a period of 2 years. The persistently infected cells were morphologically similar to the parental Vero cells and released variable amounts of infectious virus. A small percentage of the persistently infected cells produced infectious virus while a larger percentage was shown to possess viral antigens by fluorescent antibody staining. Temperature sensitivity and host cell interferon production were not involved in establishment or maintenance of persistence. The persistently infected cultures were resistant to superinfection with homologous Toscana virus, but they were susceptible to superinfection with heterologous viruses of different genera or families. Toscana virus persistently infected cells showed a selective graded resistance to the replication of other Phleboviruses. Additionally, the virus from persistently infected cells interfered with the replication of standard Toscana virus when they co-infected normal cells. The characteristics of the persistently infected cultures are compatible with some of the characteristics described for the persistence mediated by defective-interfering particles of other viruses.

Animals↗
PubMed1984

Reconstruction experiments demonstrating selective effects of defective interfering particles on mixed populations of vesicular stomatitis virus.

Mutants of vesicular stomatitis virus have previously been isolated whose replication is not affected by the presence of defective interfering (DI) particles. We describe here reconstruction experiments in BHK-21 cells which show that DI particle-resistant viruses are strongly selected over wild-type virus in the presence of DI particles. This occurs both during undiluted lytic passage and persistent infection. This selection is evident even when the mutant virus is added initially at very low levels relative to wild-type virus. This indicates that DI particles can be important selective factors affecting viral evolution.

Animals↗
PubMed1985

Persistent infection of rabies virus (HEP-Flury strain) in human neuroblastoma cells capable of producing interferon.

Apparent interferon-mediated persistent infection of rabies virus (HEP-Flury strain) was established in a human neuroblastoma SYM-I (clone K-104) cell line, which had the ability to produce interferon. This infection produced variable but small amounts of progeny virus and interferon (up to 100 IU/ml), and resisted superinfection with vesicular stomatitis virus (VSV) and Sindbis virus as well as homologous rabies virus. The treatment of this infection with anti-interferon antibody stimulated virus replication and extensive c.p.e. However, some cells survived and grew rapidly without any sign of c.p.e. These produced increased amounts (100 to 1000 times) of infectious and DI particles in the presence of anti-interferon antibody, becoming susceptible to superinfection with VSV but remaining resistant to the original rabies virus. Small plaque mutants appeared and replaced the original virus during the long-term cultivation of the persistent infection. Several mutants tested were all identified as Sdi (DI-resistant) mutants, suggesting that the persisting viruses were endowed by the Sdi mutation with a selective advantage over the original virus even in interferon-mediated persistent infections.

Animals↗
PubMed1986

Establishment of herpes simplex virus latency in vitro with cycloheximide.

Human embryonic lung cells were infected with herpes simplex virus (HSV), treated with 10 micrograms/ml or more of cycloheximide for 24 h, incubated at 37 degrees C, and then shifted to 40.5 degrees C for various periods of time (0 to 40 days) without cycloheximide treatment. No infectious virus was detected after freezing and thawing of the cultures; however, infectious virus was recovered after temperature shift-down to 37 degrees C or superinfection with human cytomegalovirus (HCMV). The time course for formation of infectious centres after temperature shift-down was examined with and without HCMV superinfection during incubation at 40.5 degrees C. Two patterns of latently infected cells were identified: one pattern showed spontaneous reactivation of virus after temperature shift-down, and the second showed reactivation of HSV after superinfection with HCMV. The first pattern showed a rapid decrease in the number of infectious centres with time, whereas the second maintained a steady reactivation rate up to 40 days at 40.5 degrees C. The same tendency was observed for infectious centre formation at 37 degrees C with and without HCMV superinfection in the HSV latency system established with (E)-5-(2-bromovinyl)-2'-deoxyuridine and interferon treatment.

Animals↗
PubMed1987

Recombinant human interferon-gamma inhibits adenovirus multiplication without modifying viral penetration.

We have recently reported that adenovirus replication is inhibited by human recombinant interferon-gamma, but not by recombinant interferon-alpha, in a dose-dependent manner. The aim of this study was to determine whether the antiviral effect of recombinant interferon-gamma could be linked to interferon-induced alteration at the membrane level, inhibiting either adenovirus penetration of or release from WISH cells. Adsorption and penetration were investigated with an 125I-labelled adenovirus binding assay. To test defective virus release, the presence of newly synthesized virus proteins in the cytoplasmic and nuclear compartments was investigated. Binding studies showed that interferons-gamma and -alpha did not modify adenovirus attachment and penetration. Interferon-gamma but not interferon-alpha inhibited hexon protein synthesis in the cytosol as well as its accumulation in the nuclear compartment. The synthesis of polypeptides III, IV and VI was also inhibited. In cells infected before interferon-gamma treatment, its addition could be delayed up to 2 h after the infection to produce an inhibition of virus yield greater than 1 log10 unit (90% inhibition). We conclude that interferon-gamma acts on an intracellular step before or at adenovirus protein synthesis, probably through a mechanism not shared with interferon-alpha.

Adenoviruses, Human↗
PubMed1994

Bovine herpesvirus 1 gIV-expressing cells resist virus penetration.

The interaction of bovine herpesvirus 1 (BHV-1) with the BHV-1 glycoprotein IV (gIV)-expressing cell line D1-1 was examined by radiolabelled virus adsorption assays, in situ autoradiography and electron microscopy. Adsorption of radiolabelled BHV-1 to D1-1 cells was similar to that observed in control cell lines but in situ radiography revealed that virus moved to the nucleus of control but not the gIV-expressing cells. Electron microscopy studies showed that BHV-1 attached to the cell membranes of D1-1 and control cells at 4 degrees C but penetration of virus was observed only in control cells when the temperature was shifted to 37 degrees C. These results provide further evidence that cellular expression of gIV does not prevent viral adsorption, but does prevent the entrance of the virus into the cell.

Animals↗
PubMed1991

Biological characterization of induced phages from Saccharopolyspora hirsuta 367 and comparison with phage JHJ-1.

Phages JHJ-2 and JHJ-3 were isolated from Saccharopolyspora hirsuta 367 UC 8106 following induction with mitomycin C and amplified on S. hirsuta NRRL B-5792. Their properties were compared with those of phage JHJ-1, isolated previously from S. hirsuta 367 NRRL 12045. The DNA restriction patterns appeared to be identical. One-step growth experiments showed no differences between the replication cycles. Burst sizes ranged from 100 to 110 p.f.u. per cell. However, the three phages showed some differences in their behaviour in different hosts. The host range of phage JHJ-1, on non-lysogenic strains, was emended to include all of the Saccharopolyspora strains tested; the host range of phage JHJ-2 was shown to be identical to JHJ-1. Phage JHJ-3 did not form detectable plaques on strains of S. rectivirgula or S. erythraea except S. erythraea NRRL 2359. Neither phage JHJ-2 nor JHJ-3 formed plaques on any lysogenic strains, while JHJ-1 formed plaques on all such strains except S. hirsuta 367 UC8106. Phage JHJ-3 was characterized as a temperate bacteriophage because it formed turbid, self-limiting plaques and lysogenized S. hirsuta NRRL B-5792. It was spontaneously released from UC8106. Both JHJ-1 and JHJ-2 formed clear and invasive (Inv+ phenotype: the property to grow on old mycelium) plaques on some Saccharopolyspora strains but clear and self-limiting plaques on others. Thus, the expression of the Inv+ phenotype encoded by JHJ-1 and JHJ-2 appears to be modulated by the host cell.

Bacteriophages↗
PubMed1980

Growth of poliovirus in HeLa cells persistently infected with HVJ (Sendai virus).

The growth of poliovirus in a HeLa cell culture persistently infected with the hemagglutinating virus of Japan (HVJ, the Sendai strain of parainfluenza 1 virus) (HeLaHVJ) was studied. Plaques produced by poliovirus on HeLaHVJ cell monolayers were hazier, smaller and fewer than those on HeLa cells. HeLaHVJ cells were indistinguishable from normal HeLa cells with respect to adsorption rate and penetration efficiency of poliovirus. Extracellular yields of poliovirus in HeLaHVJ cells were lower, and the cytopathic changes were less than those in normal HeLa cells, while cell-associated virus growth in HeLaHVJ cells was nearly equal to that in HeLa cells. HeLaHVJ cells responded more effectively to the action of magnesium chloride, which facilitates virus release from infected cells, resulting in an cytopathic effects. No reduction in poliovirus yield could be detected in HeLa cells acutely infected with HVJ. The relationship between the inhibition of the release of poliovirus from HeLaHVJ cells and the persistent infection of the cells with HVJ is discussed.

Adsorption↗
PubMed1982

Restricted viral RNA synthesis in establishment of persistent infection in Vero cells with a Sendai virus mutant.

It was previously shown that a temperature-sensitive mutant of Sendai virus, ts-23, readily establishes persistent infection in Vero cells at 37 C, a permissive temperature for growth of the mutant. In the present study, it was demonstrated that the virus yield from ts-23-infected Vero cells at 37 C began to decrease 48 to 72 hr postinfection, after an initial phase of high virus production. Before the decrease in virus production, the formation of viral nucleoprotein declined, although synthesis of all species of viral protein continued. It was suggested that the limited formation of viral nucleoprotein and the decrease in virus production were due to the restriction of viral RNA synthesis which began to occur early after infection in ts-23-infected cells at 37 C. The mutant has a temperature-sensitive defect in RNA polymerase activity and the temperature 37 C, used for establishment of persistent infection, would be a semi-permissive temperature for the RNA polymerase activity of the mutant. The ts-23 mutant interfered with the replication of the parental wild virus in Vero cells at 37 C.

Animals↗
PubMed1991

Three in-frame N-terminally different proteins are produced from the repressor locus of the Streptomyces bacteriophage phi C31.

The sequence of the repressor locus, c, of the Streptomyces temperate phage, phi C31, was shown previously to contain an open reading frame encoding a 74 kDa protein. Further analysis of the transcriptional and translational products of the c gene shows a more complex pattern of expression. A nest of three in-frame N-terminally different, C-terminally identical proteins of 74, 54 and 42 kDa were found to be expressed from a corresponding nest of transcripts. The repressor proteins were produced in Escherichia coli and the 42 kDa protein was purified, verified by N-terminal sequencing, and used to raise antibody. The antibody cross-reacted in Western blots with the 74, 54 and 42 kDa proteins expressed in E. coli and Streptomyces lividans and from Streptomyces coelicolor phi C31 lysogens. Analysis of transcription of the c gene by S1 mapping and primer extension showed that the nest of transcripts encoding the repressor protein were induced after heat treatment of the cts locus (Sinclair and Bibb, 1989; this paper). Correspondingly, all three of the repressor proteins were induced. In addition to a promoter, cp1, which lies upstream of the 74 kDa open reading frame, the c locus contained at least one internal promoter, cp2, which transcribes DNA encoding the 54 and 42 kDa proteins. Transcripts initiating from cp3 were observed in RNA preparations from S. lividans containing the c gene deleted for cp1 and cp2, but gene fusions using DNA which should contain any putative promoting activity from this region transcriptionally fused to the xylE gene showed very low levels of expression of catechol 2,3 dioxygenase in S. lividans. The 74 kDa protein was not necessary for super-infection immunity. Data described here and current knowledge of the nature of other 'dual start' genes suggest a model for the regulation of lysis versus lysogeny in phi C31.

Bacteriophages↗
PubMed1963

CIRCULATING INTERFERON IN MICE AFTER INTRAVENOUS INJECTION OF VIRUS.

Circulating interferon was detectable in mouse serum within 1 hour after the intravenous injection of various types of virus and it reached maximum levels in about 4 hours. Rapidly produced interferon may play a role in the pathogenesis of viral infection and in viral interference.

Animals↗
PubMed1992

Encoding of a homolog of the IFN-gamma receptor by myxoma virus.

Many poxvirus-encoded virulence factors have been identified as proteins that are secreted from infected cells. The major secreted protein (37 kilodaltons) from cells infected with myxoma virus is encoded by the M-T7 open reading frame. This protein has significant sequence similarity to the human and mouse receptors for interferon-gamma (IFN-gamma). Furthermore, the myxoma M-T7 protein specifically binds rabbit IFN-gamma and inhibits the biological activity of extracellular IFN-gamma, one of the key regulatory cytokines in the host immune response against viral infections.

Amino Acid Sequence↗
PubMed1985

Comparison of the airborne survival of calf rotavirus and poliovirus type 1 (Sabin) aerosolized as a mixture.

A mixture of a cell culture-adapted strain (C-486) of calf rotavirus and poliovirus type 1 (Sabin) was prepared in tryptose phosphate broth containing 0.1% uranine (physical tracer) and antifoam at a final concentration of 0.001%. By using a six-jet Collison nebulizer, the mixture was aerosolized into a 300-liter stainless-steel rotating (4 rpm) drum. The temperature of the air inside the drum was kept at 20 +/- 1 degrees C, and the virus aerosols were held at the following three levels of relative humidity (RH): low (30 +/- 5%), medium (50 +/- 5%), and high (80 +/- 5%). An all-glass impinger, containing 10.0 ml of tryptose phosphate broth with antifoam, was used to collect samples of air from the drum. Both viruses were propagated and quantitated in MA-104 cells. The calf rotavirus was found to survive well at mid-range RH, where 60% of the infectious virus could be detected even after 24 h of virus aerosolization. At the low RH, the half-life of the infectious rotavirus was ca. 14 h. On the other hand, no infectious poliovirus could be recovered from the drum air at the low and medium RH. At the high RH, more than 50% of the infectious rotavirus became undetectable within 90 min of aerosolization. In contrast to this, the half-life of the poliovirus at the high RH was about 10 h. These data, based on the aerosolization of virus mixtures, therefore suggest that there is a pronounced difference in the way RH influences the airborne survival of these two types of viruses held under identical experimental conditions.

Aerosols↗