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At least 37 records · Page 2Linked to original sources
PubMed1979

Induction of lytic plaques by murine leukemia virus in murine sarcoma virus-transformed nonproducer mouse cells persistently infected with mouse hepatitis virus MHV-S.

Kirsten murine sarcoma virus-transformed, nonproducer BALB3T3 (K-BALB) cells were persistently infected with mouse hepatitis virus, MHV-S. The cultures developed plaques after infection with murine leukemia viruses. If the murine leukemia virus-infected cultures were further submitted to the UV-XC assay, comparable numbers of XC plaques were obtained. The sensitivity to murine leukemia viruses, as determined by the UV-XC assay, was higher in MHV-S-infected cells as compared to uninfected K-BALB cells.

Animals↗
PubMed1977

Friend strain of spleen focus-forming virus is a recombinant between ecotropic murine type C virus and the env gene region of xenotropic type C virus.

The spleen focus-forming virus (SFFV), a replication-defective murine leukemia virus that causes the rapid transformation of certain hematopoietic target cells, has acquired specific xenotropic viral genetic information not contained in Friend helper virus. In the current studies, it is shown that a cDNA that represents a xenotropic virus portion of SFFV detects genetic sequences derived from the env gene region of murine xenotropic virus. The significance of the acquisition of these xenotropic viral sequences by SFFV is discussed with regard to their possible role in the rapid leukemogenicity of SFFV, and an analogy is drawn between the formation of SFFV and the formation of the Kirsten and Harvey sarcoma viruses.

Base Sequence↗
PubMed1976

Further observations on subacute sclerosing encephalitis in adult hamsters: the effects of intranasal infections with Langat virus, measles virus and SSPE-measles virus.

Passage by i.c. inoculations of suckling hamsters enhanced the virulence for adult hamsters of Langat virus (TP21), neurotropic strain of measles virus (HNT) and SSPE-measles virus (HBS), not only for i.c. infections but also for intranasal instillations. The various viral strains passaged in hamsters showed a great similarity of behaviour including the ability of producing in a proportion of apparently unaffected survivors a subacute sclerosing encephalitis, leading to atrophy of parts of the brain especially the rhinencephalon. When large groups of animals were used for transmission experiments it became obvious that within one week after intranasal exposure, all the hamsters either died or became clinically affected, or did not show signs of disease but developed acute inflammatory brain lessions. tlater on, between 2-6 weeks following inoculations only 90% of hamsters were affected with either overt signs of disease or subacute brain lesions, suggesting that in about 10% of hamsters the initial infection did not progress further and that in these animals the early brain lesions disappeared. Passage levels, irrespective of the virus used, did not influence the total numbers of infected hamsters but showed a significant effect on the mortality in TP21 and HNT infections where the number of dead and clinically affected increased in the higher passes. In these higher passes the number of survivors with subacute brain lesions decreased. In SSPE-measles virus the number of clinically affected hamsters and those surviving but developing brain lesions remained constant throughout. Vacuolated neurons were present in the brains of hamsters that survived one of the above 3 viral infections. They were seen beginning from 6 weeks after infection only in animals that developed subacute sclerosing lesions and were most commonly found in the amygdaloid nuclei and in the pyriform cortex. There was a dramatic increase in the number of brains with vacuolated neurons in hamsters infected with the high viral passes; however, in the 36th hamster passage of TP21 no vacuolated neurons were present but the total number of survivors was small, the majority had no brain lesions and none had subacute sclerosing changes.

Age Factors↗
PubMed1976

Interactions of murine leukemia virus (MuLV) with isolated lymphocytes. I. Virus replication in lymphocytes infected with Friend virus and cultures in diffusion chambers in vivo.

A new technique for infection of mature lymphocytes with murine leukemia virus (Friend) MuLV-F) is described. Spleen cells for normal, non-infected donors were placed into diffusion chambers (constructed with 0.22 mum por size Millipore filters) which were then implanted into the peritoneal cavities of normal syngeneic recipient mice. The cells were infected with an injection of MuLV-F into the peritoneal cavity and, in some instances, also by placing virus into the chambers. Cells were recovered by treating the chamber content with elastase and collagenase. The infection was determined in two ways: (1) cells with replicating MuLV were enumerated as infection centers (IC) on S+L- indicator cells; and (2) virus-related cell membrane antigen (MA) was detected by immunofluorescence. Cells recovered from chambers after 2-3 weeks of culture represented about 10% of the original inoculum; viability was approximately 90%. The number of IC in MuLV-F-infected chambers was about 10 times higher than obtained by infection and cultivation of spleen cells in vitro. The kinetics of IC and MA in chamber-cultured. MuLV-F-infected spleen cells was similar to that in the spleen of infected mice during the first 10 days after infection. Later on, the process of infection within the chambers slowed down, reaching about 50% MA-positive and about 10% IC-positive cells, whereas the number of both IC- and MA-positive cells in the spleen reached 80% or more. The infection of splenic lymphocytes in diffusion chambers occurred equally well when chambers were implanted into: (1) syngeneic, virus susceptible hosts; (2) syngeneic, lethally irradiated hosts; and (3) allogeneic, virus-resistant hosts, suggesting that the process within the chamber is independent of MuLV replication in the tissues of the chamber-bearing mouse. The diffusion chamber technique seems to provide an environment in which various types of isolated lymphocytes of different mouse strains can interact with MuLV almost as efficiently as in vivo.

Animals↗
PubMed1979

Recombination between the defective component of an acute leukemia virus and Rous associated virus O, an endogenous virus of chickens.

The ability of the defective acute leukemia virus of chickens, MC-29, to participate in recombination was investigated by testing the ability of the MC-29 genome to donate sequences to its helper virus. The endogenous virus Rous associated virus O (RAV-O) was used as a helper for MC-29, and its genome was compared by fingerprinting to that of the original RAV-O. In three separate isolates, it was found that the RAV-O used as helper for MC-29 had acquired new sequences near the 3' and 5' ends of its genome. The new 3' proximal sequences resembled the C region found in exogenous but not endogenous avian oncoviruses, and it probably imparted a higher growth rate to the recombinant as compared to RAV-O. One isolate also showed recombination within the env gene. Because we could exclude the possibility that the recombination was with host cell information or with the original helper of MC-29, we conclude that the acquired sequences were derived from the MC-29 genome, and therefore this replication defective virus is not defective in recombination.

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↗
PubMed1979

Demonstration by electron microscopy of intracellular virus in Acholeplasma laidlawii infected with either MV-L3 or a similar but serologically distinct virus (BN1 virus).

Cultures of Acholeplasma laidlawii strain M1305/68 were inoculated with Mycoplasmatales virus-laidlawii 3 (MV-L3) and examined by electron microscopy. Particles resembling MV-L3 were observed both intra- and extracellularly in thin sections prepared from MV-L3 infected cultures, but not from uninfected cultures. Similar particles were occasionally observed in uninoculated cultures of A. laidlawii strain BN1 cells, from which a virus (BN1 virus) was subsequently isolated. This virus was morphologically similar but not identical to MV-L3. It also differed serologically from, and in its resistance to, MV-L3 and the other mycoplasma viruses.

Acholeplasma laidlawii↗
PubMed1978

Generation of virus-specific cytolytic activity in human peripheral lymphocytes after vaccination with vaccinia virus and measles virus.

Human peripheral blood lymphocytes (PBL) harvested after vaccination with vaccinia or measles virus showed a specific activity against virus-infected target cells. This activity peaked on day 7 and was specific for the target cells infected with the virus used for the vaccination. The cytotoxic activity was not related to HLA markers. The cells involved in the cytolytic process were lymphocytes bearing Fc receptors. In addition, the cytotoxic activity was abrogated by more than 90% by rabbit Fab'2 anti-human IgG. It is therefore likely that two subpopulations of lymphocytes are involved: an antibody-secreting cell providing specific antiviral antibody and an effector cell bearing Fc receptor (K cells). Finally, these experiments suggest that antibody-dependent cell cytotoxicity may play a major role in the recovery from virus infection in man.

Adult↗
PubMed1976

Evaluation of Moloney murine sarcoma and leukemia virus complex as a model for airborne oncogenic virus biohazards: survival of airborne virus and exposure of mice.

Aerosols of the Moloney murine sarcoma virus (MuSV-M) and leukemia virus (MuLV-M) complex (MuSV-M/MuLV-M) were generated from refluxing atomizers and then aged in rotating drums at 21 degrees C holding temperature with relative humidities ranging from 25 to 76%. The MuSV-M and MuLV-M aerosolized from the same tumor extract preparation survived almost equally at the four humidity levels. Both viruses remained viable in the airborne state for at least 2 hours after aerosolization. When mice were exposed to airborne MuSV-M/MuLV-M, no macroscopic lesions were observed in lungs or other tissues examined during the 2-month postexposure period. On the basis of this study, MuSV-M was determined unsuitable as a "model system" in which a simple aerosol dose response could be used for biohazard evaluation of oncogenic virus aerosols.

Aerosols↗
PubMed1977

Genetic control of resistance to subgroup A and subgroup C tumour viruses in Rhode Island Red fowl: evidence for linkage between the tumour virus a (tva) and tumour virus c (tvc) loci.

A study, using the Rhode Island Red (RIR) strain of fowl maintained at Houghton Poultry Research Station, was made to investigate the genetic control of cellular response to infection with viruses of subgroups A and C. Family matings within the RIR strain and test-crosses between the RIR parents and White Leghorn (WL) parents of known ararcrcr genotype were set up to ascertain linkage between the tumour virus a (tva) and tumour virus c (tvc) loci. The results confirmed that in this RIR strain, the two loci, tva and tvc, control the cellular response to viruses of subgroups A and C, respectively, as reported in other breeds of fowl (WL and New Hampshire). As in WL fowl, the two loci are linked. The linkage value of 0-22 in the male sex agreed well with that reported in the WL male sex, indicating that the two loci are located in the same sites in homologous chromosomes in the two breeds. However, in the RIR strain, no sex difference in crossing over between the two linked loci was found, contrary to that reported in WL fowl where the absence of crossing over between the two loci was observed in the heterogametic female sex.

Animals↗
PubMed1976

Detection of neonatal calf diarrhea virus, infant reovirus-like diarrhea virus, and a coronavirus using the fluorescent virus precipitin test.

Thirty-four calf and five infant fecal specimens were tested for the neonatal calf diarrhea virus (NCDV) and for the reovirus-like infantile diarrhea agent; respectively. The procedures used were the fluorescent virus precipitin test and immune electron microscopy. Fourteen of the calf stools contained detectable NCDV, and four of the five infant stools contained the reovirus-like human agent. Infectious NCDV was detected in four of the 34 calf fecal specimens when Madin-Darby bovine kidney cell cultures that had been inoculated with supernatant fluids from stool suspensions were stained with fluorescent antibody. The 20 calf stools that did not have detectable virus were examined for the bovine corona diarrhea virus. Coronavirus was found in two of these specimens.

Animals↗
PubMedDate not supplied

[Synthesis of virus-specific products following introduction of tobacco mosaic virus RNA pereparations and the native virus into acetabularia].

The possibility to synthesize the viral-specific products after microinjection of Tobacco mosaic virus (TMV) preparations and the TMV RNA into the single-celled seaweed Acetabularia was studied. The accumulation of the newly synthesized protein and double-stranded RNA 24 hours after injection of TMV RNA and native virus preparations was demonstrated by immunological and immunofluorescent methods. The virus titer sharply dropped 3--4 hours after introduction into Acetabularia and in 48 hours it reached a maximum level. The presented data showed the possibility of TMW RNA replication and translation involving formation of viral-specific proteins and the production of a virus of full value in the Acetabularia cell.

Acetabularia↗
PubMed1977

Suppressed response to interferon inducation in mice infected with encephalomyocarditis virus, Semliki forest virus, influenza A2 virus, Herpesvirus hominis type 2, or murine cytomegalovirus.

Mice infected with encephalomyocarditis virus, Semliki Forest virus, influenza A2 virus, Herpesvirus hominis type 2, or murine cytomegalovirus developed a state of hyporeactivity to interferon induction. In general, the capacity of infected animals to produce interferon in response to inducers became progressively impaired during the course of infection. The severity and time of onset of hyporeactivity, however, were dependent upon the inducer and the nature of the viral infection. During viral infections associated with generalized hyporesponsiveness, a factor that could inhibit interferon production by murine cells in culture was identified in the serum. This serum hyporeactive factor may have mediated the development of hyporeactivity in vivo. Hyporeactivity of the host's interferon response was associated with progression of viral infection and may be partially responsible for the limited effectiveness of interferon inducers in the modification of viral infections, when administered after onset of symptoms.

Animals↗
PubMed1975

Simian virus 40-specific proteins in HeLa cells infected with nondefective adenovirus 2-simian virus 40 hybrid viruses.

The synthesis of simian virus 40 (SV40)-specific proteins in HeLa cells infected with the nondefective adenovirus 2 (Ad2)-SV40 hybrid viruses, Ad2+ND2, Ad2+ND3, Ad2+ND4, and Ad2+ND5, was investigated. Infected-cell proteins were labeled with radioactive amino acids late after infection, when host protein synthesis was shut off, and analyzed by polyacrylamide gel electrophoresis in the presence of sodium dodecyl sulfate. All polypeptides normally seen in Ad2-infected cells were found in cells infected by the hybrid viruses. In addition to the Ad2-specific proteins, cells infected with Ad2+ND2 contain two SV40-specific proteins with apparent molecular weights of 42,000 and 56,000, cells infected with Ad2+ND4 contain one protein with an apparent molecular weight of 56,000, and cells infected with Ad2+ND5 contain one protein with an apparent molecular weight of 42,000. Cells infected with Ad2+ND3 do not contain detectable amounts of proteins not seen during Ad2 infection. Pulse-chase experiments demonstrate that the SV40-specific proteins induced by Ad2+ND2, Ad2+ND4, and Ad2+ND5 are metabolically unstable. These proteins are not present in purified virions. Two nonstructural Ad2-specific proteins have been demonstrated in Ad2 and hybrid virus-infected cells which have a smaller apparent molecular weight after a short pulse than after a pulse followed by a chase. The molecular weight increase during the chase may be caused by the addition of carbohydrate to a polypeptide backbone.

Adenoviridae↗
PubMed1979

Cell surface location of simian virus 40-specific proteins on HeLa cells infected with adenovirus type 2-simian virus 40 hybrid viruses Ad2+ND1 and Ad2+ND2.

HeLa cells infected with the nondefective adenovirus type 2-simian virus 40 hybrid viruses Ad2+ND1 or Ad2+ND2 were analyzed for cell surface location of the SV40-specific hybrid virus proteins by indirect immunofluorescence microscopy. Two different batches of sera from SV40 tumor-bearing hamsters, serum from SV40 tumor-bearing mice, or two different antisera prepared against purified sodium dodecyl sulfate-denatured SV40 T-antigen, respectively, were used. All sera were shown to exhibit comparable T- and U-antibody titers and to specifically immunoprecipitate the SV40-specific proteins from cell extracts of Ad2+ND2-infected cells. Whereas analysis of living, hybrid virus-infected HeLa cells did not yield conclusive results, analysis of Formalin-fixed cells resulted in positive cell surface fluorescence with both Ad2+ND1- and Ad2+ND2-infected HeLa cells when antisera prepared against sodium dodecyl sulfate-denatured SV40 T-antigen were used as first antibody. In contrast, sera from SV40 tumor-bearing animals were not or only very weakly able to stain the surfaces of these cells. The fact that the tumor sera had comparable or even higher T- and U-antibody titers than the antisera against sodium dodecyl sulfate-denatured T-antigen but were not able to recognize SV40-specific proteins on the cell surface suggests that SV40 tumor-specific transplantation antigen may be an antigenic entity different from T- or U-antigen.

Adenoviruses, Human↗
PubMed1975

A p60 polypeptide in the feline leukemia virus pseudotype of Moloney sarcoma virus with murine leukemia virus p30 antigenic determinants.

A 60,000-dalton polypeptide (p60) has been identified in the feline leukemia virus (FeLV) pseudotype of Moloney sarcoma virus [MSV(FeLV)]. This polypeptide is present in the purified virus complex in concentrations greater than either the murine p30 or the feline p27. Purified p60 crossreacts immunologically with murine p30 group antiserum and contains several interspecies determinants, whereas the group specific determinant of FeLV p27 is not detected. Comparison of peptide fingerprints of p60 and murine p30 show many peptides in common. Limited digestion of p60 with either trypsin or chymotrypsin produced p30-35 and p20 peptides which retain the MuLV p30 group and interspecies antigenic activities. The p30 produced by both enzymes comigrates in polyacrylamide gels with the murine p30 of MSV(FeLV), thus suggesting that p60 may be an uncleaved precursor to p30.

Chromatography, Gel↗
PubMed1979

[Viruses, virus-like and virus-related structures in nasopharyngeal carcinoma (author's transl)].

Five cases of nasopharyngeal carcinoma with typically elevated EB-virus-antigen-titer were studied by light- and electron microscopic methods. Within the cytoplasm corona viruses in different forms, regular capsid-like particles with a diameter of 60 nm, tubuloreticular aggregates, and pathologic alterations of the membranes of the endoplasmatic reticulum could be found. The nuclei of the tumour cells often showed particles within the nucleoplasm with an average diameter of 100 nm containing a central core; the appearance of the particles is similar to that of herpes viruses as shown in the literature concerning EB-viruses. Atypic mitoses are common as well as free nucleoplasma-like condensates within the ground cytoplasm. Multiple doubling of the membranes of the endoplasmatic reticulum are characteristic for the tumor cell cytoplasm. Myelin figures are often situated within the enlarged tubules of the E. R., within mitochondria and within the nuclei. The results are discussed concerning the possible viral etiology of nasopharyngeal carcinoma. We do not believe that the particles found within the nucleoplasm have a relation to nuclear pores. The arguments are discussed.

Antigens, Viral↗
PubMed1978

Identification of a common antigen of herpes simplex virus bovine herpes mammillitis virus, and B virus.

In immunoelectrophoretic analyses one common antigen was demonstrated in antigen preparations from herpes simplex virus types 1- and 2- (HSV-1 and HSV-2), bovine herpes mammillitis (BHM) virus-, and B virus-infected cells solubilized by Triton X-100. The antigen was also demonstrated in solubilized purified HSV-1 and BHM virus. The common antigen was identified as antigen 11 of HSV-1 or HSV-2. Differences were found in the polypeptide composition of the related antigens when isolated from the four different herpesviruses, but a glycopolypeptide with a molecular weight of 125,000 was present in each of the four different antigen preparations, indicating that this polypeptide carried the common antigenic determinants.

Antigens, Viral↗