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At least 19 recordsLinked to original sources
PubMed1978

Immunization of mice against murine mammary tumor virus infection and mammary tumor development.

Formalin-inactivated whole murine mammary tumor virus (MuMTV), VuMTV membranes, the acid-soluble component of MuMTV, and purified MuMTV glycoprotein with a molecular weight of 55,000 (gp55; also designated as gp52) were used as vaccines in an attempt to identify the MuMTV antigen(s) that can protect mice from exogenous MuMTV infection and subsequent tumor development. Formalin-inactivated whole MuMTV, MuMTV membranes, and purified MuMTV gp55 were effective immunogens, whereas the acid-soluble component of MuMTV (which consists mainly of MuMTV gp55) failed to protect mice from challenge with live virus. These results suggest that (a) MuMTV gp55 is the major immunizing antigen and (b) its native conformation must be maintained for it to be an effective vaccine.

Acids↗
PubMed1979

Mouse mammary tumor virus infections: viral expression and tumor risk.

Concentrations of murine mammary tumor virus (MuMTV) antigen in the milk of individual naturally infected BALB/cfC3H and BALB/c mice given injections of MuMTV were related to their risk of developing a mammary tumor. Two distinct groups of MuMTV-infected mice were identified. One group exhibited high viral antigen levels in their milk (greater than or equal to 100 micrograms/ml), whereas the other group exhibited low viral antigen levels in their milk (less than or equal to 3 micrograms/ml). Mice that exhibited high levels developed tumors by 17 months of age, whereas those with low levels did not. Viral expression levels in mice having high risks of tumor development were also related to the length of the latency period preceding overt tumor development. The tumor risk potential of naturally infected mice was frequently that of their mothers. Various doses of MuMTV were injected into BALB/c mice, and the resulting infections differed in latency period, level of viral expression, and potential for neoplastic transformation.

Animals↗
PubMed1978

Melanoma skin test antigens of improved sensitivity prepared from vesicular stomatitis virus-infected tumor cells.

Crude membrane (CM) extracts from three different cultured human melanoma lines that were "virus-augmented" (infected with vesicular stomatitis virus (VSV) and subsequently inactivated by ultraviolet light) produced positive skin tests in 17 of 20 (85%), 11 of 20 (55%), and 13 of 18 (72%) tests, respectively, performed in 20 melanoma patients. Identical CM extracts from the same melanoma lines that had not been infected with VSV gave positive skin tests in 2 of 20 (10%), 4 of 20 (20%), and 2 of 18 (11%) tests, respectively, performed in the 20 melanoma patients, and no positive tests in the control patients. The 3 virus-augmented extracts were positive in only 2 of 18 (11%), 0 of 18 (0%), and 1 of 17 (6%) control subjects, respectively. The controls consisted of six normal volunteers and 12 patients with cancers other than melanoma. The "virus-augmented" CM extracts thus exhibited markedly greater sensitivity without significant loss of specificity as compared to nonvirus augmented extracts when used as tumor-specific melaonma skin test antigens.

Adult↗
PubMed1977

Body temperature and tumor virus infection. I. Tumorogenicity of Rous sarcoma virus for reptiles.

Rous sarcoma virus (RSV) was oncogenic for the following nine species of reptiles representing 6 families from Chelonia and Squamata orders: family of Testudinidae: 1. Testudo horsfieldi, family Agamidae: 2. Agama sanguinolenta; 3. Agama erythrogastra, family Lacertidae: 4. Eremias persica; 5. Eremias velox; 6. Eremias grammica, family Scincidae: 7. Eumeces taeniolatus, family Boidea: 8. Erix tataricus, 9. Ancistrodom blomhoffi. RSV did not induce tumors in 13 studied species of reptiles. Histologically 26 reptile tumors studied were polymorphous sarcomas with spindle-shaped (fibroblast-like), round and polygonal macrophage-like cells and sometimes peculiar giant polynuclear cells. Chromosomal analysis showed that reptile tumors arose out of reptile cells. RSV was pathogenic for adult reptiles. Reptile tumors did not contain a mature infectious virus. The tumors of 2 snakes were virogenic. The effect of increased temperature at the body level on the transformation of a symptomless viral infection into a viral disease is discussed in the evolutionary aspect.

Animals↗
PubMed1975

Low oncogenic potential of avian endogenous RNA tumor virus infection or expression.

Of chickens either spontaneously producing or exogenously infected in ovo with Rous-associated virus, type O (RAV-O), an endogenous virus of the chicken, only 1 died with lymphoid leukosis (LL), the most common neoplasm associated with the leukosis-sarcoma virus group. Because the chickens were not kept in strict isolation, it could not be assumed that the one LL was induced by RAV-O. In contrast, RAV-1-infected chickens from the same lines had a high incidence of LL and other neoplasms. Over 800 chickens of several inbred lines were maintained in plastic isolators free of exogenous avian leukosis-sarcoma virus infection for from 500 to nearly 1,000 days of age. No LL was observed, even though some lines are known to produce RAV-O spontaneously or to express inherited gs antigen. Three neoplasms of unknown etiology were observed, but none generally associated with leukosis virus infection. We concluded that avian endogenous virus expression had little, if any, oncogenic potential, and that exogenous avian leukosis viruses were responsible for most naturally occurring neoplasms.

Animals↗
PubMed1976

Immunity to virus-free syngeneic tumor cell transplantation in the BALB/c mouse after immunization with homologous tumor cells infected with type C virus.

Syngeneic tumor cell lines free of endogenous type C virus or viral antigen antigen expression were derived from spontaneously occurring tumors of the BALB/cCr mouse. Two cell lines free of endogenous type C virus were examined and found to be highly tumorigenic in tumor growth kinetic studies. In vitro inoculation of these cell lines with Rauscher-murine leukemia virus (R-MuLV) resulted in their chronic infection in which 95 to 100% of the cells were scored as virus positive. These infected lines showed a highly significant increase in their immunogenicity as compared to their uninfected controls. Animals in which these virus-positive tumors regressed were then shown to be highly resistant to challenge with the uninfected tumor cell lines as well as to live R-MuLV. This observed resistance to uninfected tumor cell lines could not be induced by immunization of the mouse with uninfected tumor cells and R-MuLV simultaneously at the same injection site, nor could it be induced with lethally irradiated virus-infected tumor cells, subtumorigenic doses of uninfected cells, or inactivated R-MuLV or Gross leukemia virus (G-MuLV). Cell-mediated cytotoxicity studies revealed that spleen cells obtained from animals whose virus-infected tumors regressed were cytotoxic to homologous infected and uninfected tumor cells as well as to other uninfected tumor cell lines syngeneic to the BALB/c mouse. Correlation of in vitro cytotoxicity with in vivo immunity was provided by the Winn assay, by inoculation into susceptible mice of immune and nonimmune spleen cells premixed with uninfected tumor cells. The immune cells were highly effective in preventing this tumor cell transplantation. It was concluded that type-C virus infection of these syngeneic tumor cells resulted in their acquiring strong transplantation antigens that were in part due to the virion, but were at least in part due to alterations of antigens or haptens that are present in a less immunogenic form on the uninfected tumor cell.

Animals↗
PubMed1978

Augmented immunogenicity of tumor cell membranes produced by infection with influenza virus as compared to Moloney sarcoma virus.

The tumor-associated transplantation antigens (TATA) of crude membrane extracts from SV40-transformed BALB/3T3 tumor cells lytically infected with influenza virus were markedly more immunogenic than were extracts from uninfected cells measured either by the ability to induce heightened resistance to tumorgraft challenge or by heightened lymphocyte-mediated cytotoxicity against tumor cells in vitro. When intact tumor cells (as opposed to membrane extracts) were productively infected with Moloney sarcoma virus, they were made so immunogenic that they would only grow in X-irradiated syngeneic animals. Yet crude membrane extracts from the Moloney sarcoma virus-infected tumor cells showed no increase in TATA activity analogous to that seen after infection with influenza virus. Thus, influenza virus augmentation of tumor membrane TATA may operate by a different mechanism than does the oncornavirus augmentation of intact tumor cell TATA reported by others. It appears that Moloney sarcoma virus and possibly other oncornaviruses cannot be used to augment the TATA activity of tumor cell membranes in the same way that other surface-budding viruses can.

Animals↗
PubMed1979

Bioactivities and the effect of dilution on various milk-borne murine mammary tumor viruses.

Infectivity titrations of milk-borne murine mammary tumor virus (MuMTV) from different sources or prepared in different ways or stored for periods of time have been compared. Titration curves were in general reproducible for MuMTVs of different sources or handled in different ways and for different methods of measurement, such as hyperplastic alveolar nodule (HAN) development, tumor development, or MuMTV antigen secretion in third-lactation milk, The curves had characteristic shapes with a low incidence of infection at low dilutions of milk, high incidences at intermediate dilutions, and low incidences at high dilutions. Infectivity incidences were unaffected by dilution over the range 10(-2) to 10(-5). The curves did not change appreciably with time of storage of milk at liquid N2 temperature for periods up to 3 years. Rate zonal fractionation of RIII milk gave zones with bioactivities which were not proportional to B-particle content. Upon dilution, the bioactivity of Zone 3, rich in B particles, and Zone 5, poor in B particles, increased, while the bioactivity of all the other zones usually decreased with dilution. The low incidence of infection at low dilutions may have been due, in part, to an immune response of the inoculated mouse. Administration of inactivated virions 4 h prior to or with MuMTV inoculations gave some evidence in support of this hypothesis but the complexity of the bioassay system for MuMTV lends uncertainty to interpretation of results.

Age Factors↗
PubMed1976

Augmented immunogenicity of tumor cell membranes produced by surface budding viruses: parameters of optimal immunization.

Membranes prepared from tumor cells infected with surface budding viruses are much more immunogenic than membranes from uninfected tumor cells. Factors affecting immunization with membranes from virus-infected tumor cells were studied. Preparations made with influenza virus were clearly superior to those prepared with vesicular stomatitis virus (VSV). Membranes infected with VSV were maximally immunogenic at a dose equivalent to a 10% cell pack whereas influenza-virus-infected membranes were immunogenic at 1/100th of this dose. Subcutaneous inoculation was better than other routes of administration. Maximum protection against challenge with viable tumor cells was afforded by two inoculations of VSV-infected membranes spaced 3 days apart or a single inoculation with influenza-virus-infected membranes. Administration of membranes in complete Freund's adjuvant either had no effect of induced a slight degree of tumor enhancement. Immunization with influenza-virus-infected membranes significantly reduced tumor size and incidence even at a challenge dose of tumor cells which was 50 times the LD100.

Animals↗
PubMed1977

Natural antibody in mammary tumor virus-infected mice that reacts with intracytoplasmic A particles of mouse mammary tumors.

By an indirect immunofluorescence technique with prolonged serum incubation on murine mammary tumor (MT) slices, 179 of 424 mice examined were found to possess natural serum antibody (antibodies) that reacted with intracytoplasmic A particles (iAp) of MT cells. The immunologic specificity of this antibody was supported by absorption and blocking experiments. Furthermore, a strong similarity was seen between the mouse antibody reaction on various MT and the fluorescence pattern of rabbit anti-iAp antiserum on these tumors. In female mice, incidence and geometric mean titers of the antibody in part were correlated to the spontaneous MT frequency of the mouse strains examined. Some mice of the strains XVII/Bin and CBA/BinfXVII/Bin, hitherto regarded as "free" of the mouse mammary tumor virus (MuMTV), also contained anti-iAp antibody in their sera. In contrast to MuMTV)-producing CBA/Bin micethese animals did not possess detectable spontaneous antibody reacting with MuMTV-B particles. Therefore, hypothetically, the antibody response in these mice might be induced by incomplete MuMTV expression. In the strain CBA/Bin, females 4 months old and older possessed the antibody in significantly higher geometric mean titers when compared to 4-week-old female mice. The history of lactation seemed to have no influence on the titer of antibody. In the comparatively high MT strains CBA/Bin and C3H/Bin, adult (4-month-old) females had the antibody in significantly higher levels when compared to age-matched males.

Age Factors↗
PubMedDate not supplied

Quantitative comparison of milk-released C3H and RIII mammary tumor viruses in infected BALB/c hosts.

The C3H and RIII mammary tumor viruses (MTV) carried by BALB/cfC3H and BALB/cfRIII breeding females have been quantified and compared in milk samples, after partial purification with a sucrose density gradient. The samples were collected at identical times during the first 3 lactation periods from individual mice (6 per strain), standardized for age at delivery and size of litter. Milk samples from 6 MTV negative BALB/c controls have also been analyzed. Data for comparison are expressed in optical density units (ODU) and refer to the protein content of the whole milk using MTV-negative Balb/c milk as blank. The results have shown 1) an increase of MTV released through milk in each MTV-carrying female from the first (average ODU, 0.542) to the second (1,351) and third (2.105) lactation, 2) individual variations, and 3) a significant difference in release between C3H and RIII MTV, the latter being more than double (average ODU, 1.801) in respect to the former (0.847). The apparent discrepancy between these results and the bioactivity in BALB/c mice of C3H and RIII MTV, significantly lower for the latter, is discussed.

Animals↗
PubMed1977

Immunosuppression by spleen cells from Moloney leukemia. III. Evidence for a suppressor cell that is not the leukemic, virus-producing cell.

Spleens of mice bearing MuLV (Moloney)-induced leukemia contain cells that inhibit the antibody response of normal syngeneic lymphocytes to sheep RBC in Marbrook cultures. In order to determine whether these immunosuppressive cells are virus-infected tumor cells or normal cells we pretreated leukemic spleen cell suspensions with syngeneic mouse antiserum to Moloney leukemia antigen(s) (plus complement) and with rat anti-Moloney serum (plus complement). The cytotoxic treatment killed approximately 20% to 30% and 60% to 70% of the cells, respectively. The remaining viable cell population was tested for MuLV production (in an infectious center assay on S+L-fibroblasts), for lethal effect on newborn mice, and for immunosuppressive activity. After the treatment with anti-Moloney sera the number of MuLV-releasing cells decreased 10-fold and the leukemogenic potential in vivo decreased 100-fold as compared to leukemic spleen cells pretreated with nonimmune mouse and rat sera (plus complement). In contrast, the ability of the antisera-treated cells to inhibit anti-SRBC response remained undiminished. This indicates that, in part, the immunosuppressive cells in the leukemic spleen are normal, noninfected cells, involved, perhaps, in immune regulation.

Animals↗
PubMed1979

Type C retrovirus activation and possible functions in the normal and tumor-bearing host.

The pathological consequences of tumor virus infection, transformation, and tumor development in certain experimental animals is a well-established and accepted fact. More recently, it has been suggested that these viruses may also have a physiological function participating in such processes as cellular differentiation, immune recognition, and embryogenesis. This paper delineates the current information giving some credence to physiological function for type C viruses.

Alcoholism↗
PubMed1979

Mechanism of rejection of virus persistently infected tumor cells by athymic nude mice.

Cell lines known to be tumorigenic in the nude mouse were modified by rendering them persistently infected (P.I.) with a variety of RNA viruses, including measles, mumps, vesicular stomatitis virus, and influenza. Although as few as 100 HeLa or BHK cells produced tumors in 100% of nude mice, as many as 2 x 10(7) of the same cells P.I. with viruses failed to produce tumors. An active host response responsible for restricting the growth of the P.I. cells was suggested by the findings of marked mononuclear cell infiltrates at the inoculation sites and the inability of irradiated nude mice to reject them. An analysis of the in vitro cytotoxic activity of spleen cells from normal nude mice indicated that: (a) P.I. cell lines, but not uninfected cell lines, were susceptible to spontaneous cytotoxicity; (b) in vivo inoculation of P.I. lines induced an enhanced cytotoxic activity for P.I. targets in vitro, and this induction was not specific either for inducing virus or cell line; and (c) the effector cell had the characteristics for natural killer (NK) cells. Although the specificity of recognition of the various P.I. cell lines remains unclear, cold competition experiments indicated that blocking the killing of one P.I. cell line, e.g. HeLa-measles, could be achieved only by unlabeled homologous cells, i.e. HeLa-measles, and not by uninfected cells or other P.I. lines. A variant subline of BHK cells P.I. with VSV was selected for its ability to withstand the rejection process in nude mice. These cells formed metastatic and invasive tumors in nude mice. Although they were the most potent inducers in vivo of NK cell activity against various P.I. targets, they were the most resistant of the P.I. lines to NK cell cytotoxicity in vitro. In this system there was a good correlation between tumor rejection in vivo and susceptibility to NK cells in vitro. The present results suggest that NK cells may play a significant role in both rejection of tumor cells, and in resistance to viruses, particularly persistent infections.

Animals↗
PubMed1975

Virion-associated and cellular RNA methylase activity in normal and neoplastic mammary tissue from mammary tumor virus-infected and -uninfected mice.

A comparison of cellular RNA methylase activities and patterns between normal and neoplastic mouse mammary tissue indicated the following. The rna methylases of mammary tumor tissue extracts are qualitatively different from those of normal lactating mammary tissue, based on differences in extent of methylation; the normal lactating tissue extracts have a greater capacity of methylate RNA than do the tumor extracts studied to date. There is no correlation between capacity and either the malignant state or the etiological agent. There is a qualitative effect on methylation patterns attributable to the presence of virus. Finally, both the etiological agent, mouse mammary tumor virus, and its putative nucleoprotein core, intracytoplasmic A particles, have a N-2-guanine RNA methyltransferase integrally associated with them. These conclusions are consistent with the aberrant nucleic acid methylation hypothesis, with the reservation that aberrant does not imply hypermethylation.

Animals↗
PubMed1976

Murine mammary tumor virus: characterization of infection of nonmurine cells.

Murine mammary tumor virus (MuMTV) was used to productively infect feline and mink cells. MuMTV "proviral" DNA could be detected in the infected cells by molecular hybridization using radioactive MuMTV complementary DNA as a probe. Kinetic analysis of MuMTV proviral DNA synthesis after infection showed that maximum MuMTV DNA synthesis was achieved by 8 h; however, this was followed by a decline in detectable proviral DNA and eventual stabilization at a lower level. MuMTV synthesis in feline cells was greatly stimulated by the synthetic glucocorticoid, dexamehtasone. On the other hand, MuMTV synthesis in mink cells was relatively at a much higher level in absence of dexamethasone and the stimulation with dexamethasone was not as marked as in the case with infected feline cells. Thermal denaturation of hybrids between MuMTV complementary DNA and infected mink cell RNA revealed no difference from homologous hybrids.

Animals↗