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Biomedical subjects

S K Datta

Publications and source records attributed to S K Datta.

At least 127 records · Page 7Linked to original sources
PubMed1978

Restricted expression of ecotropic virus by thymocytes of leukemia-resistant (AKR X NZB)F1 mice.

AKR mice, which produce high titers of ecotropic virus, were crossed with NZB mice, which produce titers of xenotropic virus. Spleen, marrow, and lymph node cells of the F1 hybrid produced high titers of ecotropic and xenotropic viruses. However, expression of ecotropic virus by both thymus cells and peripheral T cells of the F1 was severely restricted. Despite simultaneous expression of ecotorpic and xenotropic viruses in F1 spleens, lymph nodes, and marrows evidence for recombinant viruses was not found. Such viruses were also undetectable in the F1 thymuses. The results indicate that a cellular mechanism, present in AKR thymus but lacking in the F1 influences virus expression and the formation of recombinant viruses. This may account for the low incidence of leukemia in the F1 hybrid.

Animals↗
PubMed1978

Genetic studies of autoimmunity and retrovirus expression in crosses of New Zealand black mice I. Xenotropic virus.

The relationship between expression of xenotropic virus and the development of autoimmunization was studied in the progeny of crosses between New Zealand Black (NZB) and SWR mice. The (F1 X SWR) and F2 progeny segregated into three phenotypes: high-virus, low-virus, and virus-negative; F1 and (F1 X NZB) progeny were always high-virus. Autoantibodies, immune deposit nephritis and lymphomas developed in the progeny of these crosses. The virological phenotype of the animal could be dissociated from the presence of either autoantibodies or nephritis. For example, mice that expressed titers of virus as high as the NZB parent failed to develop signs of autoimmunization, even up to 24 mo of age. By contrast, some (F1 X SWR) and F2 mice that expressed low titers of virus developed autoimmune disease. Furthermore, a proportion of virus-negative mice produced autoantibodies and were found to have typical immune deposit nephritis. No viral antigens could be detected in the renal lesions of such virus-negative animals. By contrast with the dissociation between expression of virus and occurrence of nephritis, the presence of antibodies to DNA correlated with the development of renal lesions. We conclude that the genes that determine the expression of infectious xenotropic virus in NZB mice segregate independently from those that are involved in the autoimmune disease of these animals.

Animals↗
PubMed1978

Genetic studies of autoimmunity and retrovirus expression in crosses of New Zealand black mice. II. The viral envelope glycoprotein gp70.

The retroviral envelope glycoprotein, gp70 was measured in the serum of New Zealand Black (NZB) and SWR mice and the progeny of their crosses. The serum gp70 values segregated to "NZB-like" and "SWR-like" levels in these mice. A complex mechanism determined the inheritance of NZB-like serum gp70 levels. We found that the factors determining the expression of this retroviral protein were independent of the genes (Nzv-1 and Nzv-2) that determined the expression of infectious xenotropic virus. Autoimmune disease, including immune deposit nephritis could be dissociated from the degree of expression of serum gp70. By contrast, presence of circulating immune complexes and anti-DNA antibody did correlate with the development of nephritis in these crosses. A significant correlation was found between high grade expression of serum gp70 and the presence of lymphomas in these mice.

Animals↗
PubMed1978

Xenotropic virus and autoimmunity in NZB mice.

The high-grade expression of xenotropic virus in NZB mice is determined by two autosomal dominant loci (Nzv-1 and Nzv-2). The progeny of crosses between NZB and the "nonautoimmune" virus-negative SWR strain segregate into three phenotypes: high-virus, low-virus, and virus-negative. The virologic phenotypes of the animals could be dissociated from the presence of either autoantibodies or immune complex-deposit nephritis and the latter could develop in the crosses without deposits of viral antigens in the glomeruli.

Animals↗
PubMed1975

Splenocyte plaque assay for the detection of murine leukemia virus.

A modified XC assay for murine leukemia virus (MuLV) employing splenocytes taken directly from the animal is described. This modification can be more than 1000 times more sensitive than XC plaque assays employing tissue extracts. This technique should lend itself readily to the quantitation of infectious MuLV in defined populations of lymphoid cells.

Animals↗
PubMed1975

Lymphocytes and leukemia viruses: tropism and transtropism of murine leukemia virus.

The tropism of naturally occurring murine leukemia virus (MuLV) was investigated in short-term lymphocyte cultures. The tropism of MuLV was readily defined in fibroblast cultures, but not in lymphocyte cultures. Lymphocytes free of infectious MuLV could be infected across the tropism barrier by partially purified MuLv or by in vitro contact with MuLV-producing lymphocytes. Stimulation of lymphocytes was not required for this cross-infection and replication of MuLV. When cross-infected lymphocytes and was specifically associated with lymphocytes were stimulated in vitro by allogeneic cells, they facilitated MuLV infection of ordinarily non-permissive fibroblasts. This phenomenon (transtropism) required antigenically stimulated lymphocytes and was specifically associated with infection of the lymphocyte by MuLV across the tropism barrier. Thus in contrast with the resting lymphocyte, the transformed lymphocyte acquired the ability to disseminate infectious MuLV to nonpermissive cells. These findings suggest a novel relationship between lymphocytes and leukemia viruses. They indicate one mechanism whereby antigenic stimulation may enhance the development of virus-induced lymphoid neoplasms.

Animals↗