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At least 19 recordsLinked to original sources
PubMed1975

Virus development in enucleate cells: echovirus, poliovirus, pseudorabies virus, reovirus, respiratory syncytial virus and Semliki Forest virus.

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.

Autoradiography↗
PubMed1975

Multiple sclerosis and parainfluenza 1 virus. History of the isolation of the virus and expression of phenotypic differences between the isolated virus and Sendai virus.

54 cultures were established from brain tissue obtained 2-3 hrs after death from 1 case of multiple sclerosis and 30 cultures from another case. Following fusion with indicator cells in the presence of lysolecithin, a parainfluenza type 1 virus (6/94 virus) was isolated from cultures representing one plaque area in the first case and one plaque area in the second case. A cell line chronically infected with the 6/94 virus has been maintained for more than 100 passages in vitro. A close relationship to the Sendai Hemagglutinating Virus of Japan (HVJ) is indicated from RNA-RNA hybridization and the patterns of electrophoretic mobilities of viral polypeptides. Conversely, differences in optima for growth-requirement temperatures, hemolytic activity and the capability to fuse mammalian cells, distinguishes 6/94 virus and HVJ as distinct phenotypic entities of a closely related genotype.

Adult↗
PubMed1975

Separation of sarcoma virus-specific and leukemia virus-specific genetic sequences of Moloney sarcoma virus.

We have studied the nucleic acid sequences in nonproducer cells transformed by Moloney sarcoma virus or Abelson leukemia virus (two types of replication-defective, RNA-containing, viruses isolated by passage of Moloney leukemia virus in BALB/c mice). DNA probes from the Moloney leukemia in virus detect RNA in both Abelson virus-transformed nonproducer cells and Moloney sarcoma virus-transformed nonproducer cells. A sarcoma-specific cDNA, prepared from the Moloney sarcoma virus, has extensive homology to RNA found in heterologous nonproducer cells transformed by Moloney sarcoma virus, has little homology to RNA in cells producing Moloney leukemia virus, and no detectable homology to RNA in nonproducer cells transformed by the Abelson virus. By analogy to earlier data on avian and mammalian sarcoma viruses, these results suggest that the Moloney sarcoma virus arose by recombination between a portion of the Moloney leukemia virus genome and additional sarcoma-specific information, and indicate that the expression of this information in not essential for Abelson virus-mediated fibroblast transformation.

Cell Line↗
PubMed1978

The entry into host cells of Sindbis virus, vesicular stomatitis virus and Sendai virus.

We have compared the mechanisms of entry into host cells of three enveloped viruses: Sendai virus, vesicular stomatitis virus (VSV) and Sindbis virus. Virus entry by membrane fusion should antigenically modify the surface of a newly infected cell in such a way that it will be killed by anti-viral antibody and complement. On the other hand, virus entry by a mechanism involving uptake by the cell of the whole virion should not make cells sensitive to antibody and complement. As expected, cells newly infected with Sendai virus were readily and completely lysed by anti-Sendai antibody and complement. In marked contrast, however, cells newly infected with either Sindbis virus or VSV were killed by anti-viral antibody and complement only when infected at an extremely high multiplicity of infection, in excess of 1000 plaque-forming units per cell. We favor the following explanation for these results with Sindbis virus and VSV: a very large majority of the Sindbis and VSV virions entered the infected cells by some means other than membrane fusion, presumably engulfment of the whole particle. Efficient entry by way of membrane fusion may therefore not be a general characteristic of enveloped viruses.

Antigens, Surface↗
PubMed1979

Wild mouse RNA tumor viruses. A nongenetically transmitted virus group closely related to exogenous leukemia viruses of laboratory mouse strains.

Type-C RNA viruses isolated from wild mice are causative of naturally occurring neoplasia and neurologic diseases. Biochemical and immunologic characterization of this virus group revealed that amphotropic viruses isolated from wild mice trapped in separate geographical areas are indistinguishable, whereas amphotropic and ecotropic viruses naturally infecting the same animal are env gene variants. Molecular hybridization studies established that neither host range variant is endogenous to the Mus musculus genome, although each demonstrates partial nucleotide sequence homology. Wild mouse type-C viruses exhibited much closer molecular and antigenic relatedness to the exogenous virus subgroup (Friend-, Moloney-, and Rauscher-MuLV) than to prototype endogenous viruses isolated from laboratory mouse strains. The evidence indicates that exogenous mouse type-C viruses have been maintained in nature over a long period of evolution as a separate virus group, causative of tumors in mice by a mechanism solely involving their transmission as infectious agents.

Animal Population Groups↗
PubMed1976

Sialylatin of glycoproteins of murine mammary tumor virus, murine leukemia virus, and Mason-Pfizer monkey virus.

Neuraminidase treatment of mouse mammary tumor virus, Rauscher murine leukemia virus, and Mason-Pfizer monkey virus resulted in loss of their capacity to inhibit hemagglutination of influenza virus. Hemagglutination-inhibition activity of these RNA tumor viruses could be restored by in vitro resialylation catalyzed by sialyl transferase. The major glycoprotein in the intact envelope of desialylated and, to some extent, native virions could be specificallly labeled in vitro with CMP-(14C) sialic acid. These studies further characterize the individual glycoproteins of mouse mammary tumor virus, Rauscher murine leukemia virus, and Mason-Pfizer monkey virus.

Animals↗
PubMedDate not supplied

Cross-protection between Tacaribe complex viruses. Presence of neutralizing antibodies against Junin virus (Argentine hemorrhagic fever) in guinea pigs infected with Tacaribe virus.

Cross-protection between Junin virus and five other Tacaribe complex viruses and the serological response of guinea pigs inoculated with Tacaribe virus are reported here. Previous infection with Tamiami or Pichinde viruses significantly delayed guinea pig deaths. A 58% survival rate was found among animals immunized with three doses of Amapari virus, while guinea pigs inoculated with one dose of Machupo or Tacaribe virus were fully protected against Junin virus. Neutralization tests performed in serum samples of guinea pigs immunized with five doses of Tacaribe virus showed that they developed monologous and heterologous neutralizing antibodies.

Animals↗
PubMed1975

Aberrant viruses in cells infected with murine sarcoma virus-feline leukemia virus.

This study describes an unusual type of virus seen when a feline leukemia virus (FeLV) pseudotype of murine sarcoma virus (MuSV) obtained by cocentrifugation procedures infected feline embryo cells (FEF) and two Crandell cat cell lines (CrFK1, CrFK2). When all three cell cultures were infected with MuSV-FeLV, only FEF and CrFK2 were transformed and only these showed normal and aberrant virus. The CrFK1 infected with MuSV-FeLV did not transform but did replicate normal type-C virus with a 50-A intermediate coat. The virus replicated in the two transformed lines showed three particles; a normal particle with a 50-A intermediate coat, a normal particle with a 100-A intermediate coat, and an aberrant particle with a 100-A intermediate coat.

Animals↗
PubMed1978

Effect of interferon on mouse cells chronically infected with murine leukaemia virus: kinetic studies on virus production and virus RNA synthesis.

NIH/3T3 cells chronically infected with the Moloney strain of murine leukaemia virus were incubated with interferon (IF). There was no effect on virus production during the first 4 h, but thereafter an antiviral state gradually developed, reaching a maximum at about 12 h. When IF was removed, the antiviral state (expressed in terms of inhibition of release of virus) remained constant for 10 h, after which there was an abrupt return to the normal rate of virus release. Analysis of IF-treated cells showed that there was a three to fourfold increase in the amount of virus RNA in the nucleus at 48 h after IF addition, and still a slight increase at 72 h. There were no increases in the amounts of virus RNA in the cytoplasm during 72 h after the addition of IF. These results agree with the postulate that IF inhibits a late stage in the maturation of virus in chronically infected cells.

Animals↗
PubMed1979

Establishment of a C3Hf mammary tumor cell line expressing endogenous mouse mammary tumor virus: antigenic and genetic relationships of this virus with highly oncogenic mouse mammary tumor viruses.

A single-cell clone of C3Hf mammary tumor cells (clone 14) was developed into a continuous cell line expressing high levels of endogenous mouse mammary tumor virus (MMTV) with less than 0.1% murine leukemia virus expression. Comparison of the C3Hf MMTV protein profile on sodium dodecyl sulfatepolyacrylamide gel electrophoresis with that of C3H MMTV revealed that the protein content of the two viruses was quite similar. However, oligonucleotide fingerprints obtained of MMTV 70S RNA revealed that approximately 20% of the large oligonucleotides examined were unique to each virus. The oligonucleotide fingerprint indicated that although the viruses were similar, they differed in their genetic content. The differences in the two viruses extended to immunological differences in the major envelope glycoprotein, gp52. C3Hf MMTV competed only partially in a homologous radioimmunoassay for gp52 of C3H MMTV, whereas C3H MMTV gave complete competition, indicating that gp52 of C3H MMTV contained type-specific determinants not present on gp52 of C3Hf MMTV. Comparison of C3Hf MMTV with highly oncogenic C3H, GR, and RIII MMTVs in a homologous C3H MMTV gp52 assay gave two patterns of reactivity: complete competition by GR and C3H MMTV and incomplete competition by C3Hf and RIII MMTV. Absorption of anti-C3H MMTV serum by either C3Hf MMTV or RIII MMTV removed all antibodies against both viruses but not against GR and C3H MMTVs. These results indicate that C3H and GR MMTVs are more closely related to each other than to RIII and C3Hf MMTVs.

Animals↗
PubMed1977

[Differentiation of type D virus from continuous human cells (Il'in-Bykovskiĭ virus) and Mason-Pfizer monkey virus by the antigens of the viral envelopes].

For differentiation of Ilvin-Bykovsky virus (IBV) and monkey Meson-Pfeizer virus (M-PMV) the method of virus neutralization with antibodies against the envelope virus antigen was used. The viruses were cultivated in similar human embryo cells. The results of the virus neutralization were determined by presence or absence of the gs-antigen in the infected cells. The antiserum to M-PMV envelope antigens did not neutralize the IBV antigen. It has been concluded that IBV and M-PMV differ by their envelope antigens and should be regarded as different viruses.

Animals↗
PubMed1979

Evolutionary relationships of the primate papovaviruses: base sequence homology among the genomes of simian virus 40, stump-tailed macaque virus, and SA12 virus.

Physical maps of the genomes of the two newly discovered primate papovaviruses, SA12 and stump-tailed macaque virus (STMV), were generated by restriction endonuclease analysis. The base sequence homologies among the genomes of SA12, stump-tailed macaque virus, and simian virus 40 (SV40) were studied by heteroduplex analysis. Heteroduplexes between SA12 and SV40 DNAs and stump-tailed macaque virus and SV40 DNAs were constructed and mounted for electron microscopy in various amounts of formamide to achieve a range of effective temperatures. At each effective temperature, the regions of duplex DNA in the heteroduplexes were measured and localized on the SV40 physical and functional maps. By analyzing the data from this study and rom our previous study (N. Newell, C. J. Lai, G. Khoury, and T. J. Kelly Jr., J. Virol. 25:193-201, 1978) on the base sequence homology between the genomes of BK virus and SV40, some general conclusions have been drawn concerning the evolutionary relationships among the genomes of the primate papovaviruses. The extent of homology among the viral genomes does not reflect the phylogenetic relationships of their hosts. At comparable effective temperatures Tm - 33 degrees C), the heteroduplexes between the DNAs of BK virus and SV40 contained the largest amount of duplex (about 90%). The heteroduplexes made between SA12 and SV40 DNAs were slightly less homologous, containing about 80% duplex. The heteroduplexes made between SV40 and stump-tailed macaque virus DNAs were only 20% duplex under the same conditions. When the various heteroduplexes were mounted for microscopy at effective temperatures greater than Tm - 33 degrees C, the fraction of the duplex DNA decreased in each case, indicating the existence of considerable base mismatching in the homologous regions. When specific coding or noncoding regions of the viral genomes were compared, the data indicated that the extent of sequence divergence differed markedly from one region to another. In all the heteroduplexes studied, there were two regions, located near the junctions between early and late regions on the SV40 map, which were essentially nonhomologous. All of the heteroduplexes studied showed significantly greater homology in the late region than in early region. Within the late region, the sequences coding for the major capsid polypeptide, VP1, were the most highly conserved.

Base Sequence↗
PubMed1976

Avian leukosis viruses of different subgroups and types isolated after passage of Rous sarcoma virus-Rous-associated virus-0 in cells from different ring-necked pheasant embryos.

Avian leukosis viruses of subgroups A and F (RAV-A and RAV-F) arose at a low rate after passage of Rous sarcoma virus-Rous-associated virus-0, which is subgroup E, in cells from ring-necked pheasant embryos. In cells of two embryos, all of the viruses isolated after virus passage were RAV-F. However, in cells of a third embryo, both RAV-A and RAV-F were isolated. In addition, there sometimes were type-specific differences among the different isolates of RAV-A and RAV-F from the cells of single embryos. These results indicate that the RAV-A and RAV-F probably arose by recombination of viral and cellular genes, that different ring-necked pheasant embryo may have different endogenous avian leukosis virus-related nucleotide sequences, and that recombination at different sites in these endogenous sequences might give rise to type-specific differences among the RAV-A and RAV-F.

Animals↗
PubMed1978

Oncogenicity of the C-type virus HL-23V in marmosets and characterization of virus isolated from an HL-23V-induced marmoset tumor: comparison with simian sarcoma virus type 1.

Dog thymus cells chronically infected with HL-23V, a C-type virus isolated from human acute myelogenous leukemia cells, produced both transforming and nontransforming virus indistinguishable from simian sarcoma virus type 1 (SSV-1/SSAV-1) and induced fibromas in newborn marmosets. All inoculated marmosets developed anti-HL-23V antibodies. A cell line established from a tumor biopsy produced transforming virus identical to SSV-1 and HL-23V at early passages. However, at later passages the cell line and a cell line established from residual tumor tissue removed at autopsy, produced virus which was neutralized only at low dilutions of anti-SSV-1 serum (1:32) relative to SSV-1 (1:1,024). This virus (BFV) was also distinguished from SSV-1 and HL-23V by XC tests, and by membrane immunofluorescence and serum cytotoxicity tests.

Animals↗
PubMed1978

The analysis of the monoclonal immune response to influenza virus. III. The relationship between stimulation of virus-primed precursor B cells by heterologous viruses and reactivity of secreted antibodies.

Individual splenic precursor B cells from BALB/c mice primed with influenza virus PR8[A/PR/8/34 (H0N1)] were stimulated in vitro in the splenic fragment culture system by homologous or various heterologous influenza viruses. The specificity of the stimulated precursor cells was determined by analysis of the antibodies secreted by the ensuing plasma cell clone in a radioimmunoassay (RIA). Viruses of the H2N2 and H3N2 subtypes were unable to stimulate hemagglutinin (HA)- or neuraminidase (NA)-committed precursor B cells but did efficiently stimulate chicken host component (ChHC)-committed precursors. Viruses of the H1N1 and H0N1 subtypes could stimulate precursors committed to any of the three viral surface components. Analysis of the fine specificity of HA-committed B cells showed that BEL(H0N1) and CAM(H1N1) stimulated almost exclusively precursors whose clonal antibody product reacted with the stimulating virus in the RIA. On the other hand, WSE and MEL (both H0N1) quite frequently were able to stimulate precursors whose clonal antibody product did not react with the stimulating virus in the RIA. These results suggest that the stimulatory interaction of viruses with the cell-bound immunoglobulin receptors is slightly less affinity dependent than the antigen-antibody interaction in the RIA.

Animals↗
PubMed1978

Immunological studies of heat-labile virus inhibitors. I. Specificity of absorption onto sensitive viruses and specific response after virus infections.

Heat-labile virus inhibitor (HLI) in normal sera of various mammalian species capable of neutralizing variola (VRV) and Newcastle disease viruses (NDV) was studied immunologically. After sucrose density gradient centrifugation of guinea pig serum, the HLI activity against VRV and that against NDV were both demonstrated in the same region sedimenting fastor than IgM. Absorption with partially purified VRV or NDV removed the HLI activity on the homologous virus but not that on the other. Prior saturation of virions with specific antibody blocked the absorption of HLI, suggesting a specific competition for binding site (s) between specific antibody and HLI. The HLI level against variola virus was checked in connection with immunization with vaccinia virus. In human primary vaccination, the HLI level rose sharply within 4 weeks after vaccination, turning to decline gradually to settle at a level higher than that of the conventional neutralizing antibody (NA). In cases of human revaccination, a sharp rise of HLI started 4 days after vaccination and reached the highest level within 7 days, preceding the rise of conventional NA level which occurred about 3 days later. Three rabbits with negative HLI activity prior to vaccinia immunization obtained an HLI activity within 2 weeks, which showed a sharp rise up to 6-8 weeks. One rabbit with a positive prior HLI activity also showed a sharp rise of the HLI activity after immunization. In all rabbits the final HLI level was identical with that of conventional NA. Groups of guinea pigs were immunized with either VRV or NDV. Rises of the HLI level after immunization were observed in all animals, the activity being restricted to the homologous virus used in the immunization. Complement requiring NA was detected during the course of immunization but its behavior was different from that of HLI. The above observations were interpreted to suggest a ubiquitous presence of HLI as a specific reactive agent and its role at an earliest stage of immune response.

Absorption↗