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PubMed1983

Expression and disposition of the murine mammary tumor virus (MuMTV) envelope gene products by murine mammary tumor cells.

Three murine mammary tumor virus (MuMTV)-producing epithelial cell lines derived from murine mammary tumors were examined in order to identify the MuMTV-specific cell surface antigens and their distribution on the cell surface, to study the kinetics of the MuMTV envelope precursor processing, virus assembly, and release, and to characterize the soluble MuMTV antigens that are shed into culture medium. Cell surface labeling experiments showed that only the mature MuMTV envelope glycoproteins gp52 and gp36 were exposed on the cell surface, and that gp52 was more abundant than gp36. In cells producing large quantities of MuMTV, expression of gp52 on the cell surface was shown by immunoelectron microscopy to be localized predominantly on the surface of budding virions and not on smooth areas of the cell surface where virus was not budding. The cell surface associated gp36 was found not to be incorporated into budding virions. A few cells in all three cell lines were found to produce only a few or no MuMTV particles and in these cells, unlike in the high virus-producing cells, considerable quantities of gp52 were expressed on the surface membrane. All three cell lines were found to shed large amounts of the MuMTV env precursor polyprotein as well as the mature non-virion-associated glycoprotein, gp52, into the culture medium. The envelope precursor protein (P75env) that was shed into the culture medium was found to differ from the predominant form of the cellular env precursor (Pr70env) in that (1) P75env migrated with an apparent higher molecular weight than Pr70env in SDS gels; (2) Pr70env contained only the core oligosaccharide, whereas P75env contained fucose in addition to the core sugars; (3) two-dimensional gel electrophoretic analysis showed that Pr70env could be resolved into three to four components migrating in the basic region of the isoelectric focussing gel (pH 7-8), whereas P75env was resolved into 9-13 components migrating in a more acidic region of the gel (pH 5-7). The molecular structure of the exfoliated gp52 was found to be similar to that of the gp52 that was incorporated into the virions although the virion-associated gp52 was not the source of the gp52 in the medium. Our quantitative pulse-chase studies suggest that of the two populations of MuMTV env precursors that are present in MuMTV-producing cells, only Pr70env is processed intracellularly to give rise to the mature MuMTV envelope proteins gp52 and gp36.

Animals↗
PubMed1984

Mouse mammary tumor virus can mediate cell fusion at reduced pH.

Mouse mammary tumor virus, a type-B retrovirus, was shown to mediate fusion of cultured cells following low-pH treatment. Fusion could be demonstrated both with virus-infected cells or with uninfected cells carrying freshly absorbed virus. Although the fusion response was variable between different cell lines, one line of MMTV-infected mink lung cells, designated MGR4, was particularly susceptible to fusion at reduced pH. Since expression of MMTV in these cells is strongly regulated by glucocorticoids, it was possible to demonstrate that cell fusion was dependent on MMTV-encoded functions. With MGR4 cells, a pH threshold for membrane fusion was observed, centered on pH 5.5, at which 50% of the cells were fused. At lower pHs virtually all of the cells in the monolayer fused. These results are similar to those described for other virus groups and are consistent with the idea that most enveloped animal viruses infect cells by a common mechanism involving membrane fusion triggered by low pH.

Animals↗
PubMed1985

Molecular basis of altered mouse mammary tumor virus expression in the D-2 hyperplastic alveolar nodule line of BALB/c mice.

The preneoplastic D-2 hyperplastic outgrowth line, which was derived from a hormone-induced hyperplastic alveolar nodule (HAN) of a BALB/c mouse, was used for a detailed analysis of mouse mammary tumor virus (MMTV) expression. The D-2 HAN line has previously been shown to express viral RNA representative of the entire genome, although viral particles have been noted only rarely. The MMTV-specific mRNA, protein, and DNA content of the D-2 tissues was defined in an effort to better understand the molecular basis of the aberrant virus expression. Northern blotting techniques demonstrated the presence of properly processed 8.9 kb (genomic) and 3.6 kb (envelope) mRNA. Protein electroblotting procedures established the presence of properly processed viral core protein p28. In contrast, the envelope precursor polyprotein was not processed into detectable levels of gp52. Analysis of MMTV proviral content by Southern blot methodology revealed the presence of a newly acquired provirus which serves as a marker for the clonal nature of the D-2 line. The origin of the new provirus is unknown. Methylation studies established that the new proviral insert is hypomethylated and, therefore, is likely serving as the template for the MMTV expression observed in the D-2 HAN line. These characteristics of the D-2 line make it an excellent system in which to study the role, if any, of MMTV in the progression of D-2 preneoplastic tissues to the tumor phenotype.

Animals↗
PubMed1985

Identification and characterization of a mouse mammary tumor virus protein uniquely expressed on the surface of BALB/cV mammary tumor cells.

A unique subline of BALB/c mice, designated BALB/cV, exhibits an intermediate mammary tumor incidence (47%) and harbors a distinct milk-transmitted mouse mammary tumor virus (MMTV). The BALB/cV subline was used to study the molecular basis of potential virus-host interactions involving cell surface-expressed MMTV proteins. Cell surface iodination identified virus-specific proteins expressed on BALB/cV primary mammary tumor cells grown in culture. In contrast to (C3H)MMTV-producing cell lines which expressed MMTV gp52, BALB/cV tumor cells lacked gp52 and expressed instead a 68K, env-related protein. The 68Kenv protein was also detected on the surface of metabolically labeled BALB/cV tumor cells by an external immunoprecipitation technique. The expression of 68Kenv was restricted to mammary tissues of BALB/cV mice that also expressed other MMTV proteins. Biochemical analysis established that 68Kenv was not modified by N-linked glycosylation. 125I-labeled 68Kenv was rapidly released into the media of tumor cell cultures and was recovered both in the form of a soluble protein and in a 100,000 g pellet. The biologic function of this cell surface-expressed viral protein remains unknown.

Acetylglucosaminidase↗
PubMed1987

A rare common integration site of proviruses of the mouse mammary tumor virus in P-type mammary tumors of mouse strain GR.

The mouse mammary tumor virus (MMTV) can induce mammary tumors in mice by proviral activation of the cellular oncogenes int-1 or int-2. Activation of these genes, however, is observed in only a few hormone- and pregnancy-dependent mammary tumors of the mouse strain GR. To study the possible involvement of other oncogenes we cloned three MMTV proviral-host fragments (MT 40, 42, and 53) from different mammary tumors of GR with a single acquired MMTV provirus. From a genomic library of normal mouse DNA we isolated phages with insert DNAs that covered 20-30 kb of the uninterrupted regions. Suitable probes devoid of repetitive DNA sequences were isolated in order to screen other mammary tumors for MMTV proviral integrations in these regions. Only two mammary tumors, MT 40 and 42, showed integration of extra MMTV proviruses within the same region. The integrations occurred only 60 bp apart. The other mammary tumors, however, did not contain MMTV proviral integrations in this region, nor in the MT 53 region. Using mouse-hamster somatic cell hybrid DNA, the MT 40/42 integration region was assigned to mouse chromosome 7, and the second region, MT 53, to chromosome 16. The two regions bear no homology to known cellular oncogenes. We did not observe any mRNA being expressed from these cloned segments either in tumors or in normal mammary glands. These findings indicate that plaque(P)-type mammary tumors in mouse strain GR do not originate from MMTV provirus insertions in a particularly favored integration region, but that there may be a variety of integration sites in these tumors.

Animals↗
PubMed1990

Virus envelope-based peptide vaccines against virus-induced mammary tumors.

Previous studies by us and others established that mammary tumors induced by murine mammary tumor virus (MuMTV) could be prevented to various extents by prior vaccination with MuMTV-containing or subviral component immunogens. In this report, four predicted surface-accessible peptide regions (EP-1 to EP-4) of the major viral envelope glycoprotein (gp52) of C3H-MuMTV were tested as carrier-conjugated vaccines for the protection of Balb/c mice against a live virus challenge. With tumor incidence as an endpoint, vaccination with one of these synthetic peptides (EP-3) resulted in a significant reduction in the frequency of early onset tumors and 67% of the test animals remained tumor-free for the entire observation period (16 months). In contrast, only marginal protection was obtained by immunization with the intact glycoprotein (gp52). Immunologic interference may explain the lower protective efficacy of gp52, as compared to EP-3.

Amino Acid Sequence↗
PubMed1987

Age related differences in immunocompetence and incidence of mammary adenocarcinoma in murine mammary tumor virus-infected C3H/Bi mice.

In breeder C3H/Bi female mice, infected neonatally by murine mammary tumor virus (MTV), the incidence of spontaneous mammary tumors is greater than 95% between 5 and 9 months of age. In young (2-3 months) female the probability for developing a tumor in the next month is negligible, higher than 80% in mice of middle age (5-6 months) but lower than 4% in aged (10-12 months) females. The age-related changes of some immune functions of spleen cells from these tumor free female mice have been evaluated. While the proliferative capacity of cells to Phytohemagglutinin (PHA) increases, the T cell-dependent antibody response against sheep red blood cells (SRBC) and the antibody-dependent cellular cytotoxicity (ADCC) are significantly decreased in 5-6-month-old mice as compared to the young (2-3 months) female mice. The antibody response against SRBC and the mitogenic response to PHA decline markedly in 10-12-month-old mice but the ADCC increases in this group of mice. In addition, assays with monoclonal anti-Lyt-1 and anti-Lyt-2 antibodies indicate that percentage of Lyt 1- 2+ cells (suppressor and cytotoxic T cells) is lower in 10-12-month-old female as compared to 5-6-month-old animals. These results show that the immune alterations observed in 10-12-month-old C3H/Bi mice are not closely associated with an increase in incidence of spontaneous tumors and suggest that a high non-T killer cell activity could protect some of these older C3H/Bi female mice against mammary tumor development.

Aging↗