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  • Title: Leporine acquired immune deficiency disease.
    Author: Sell S, Strayer D, Skaletsky E, Corbeil L, Cabirac G, Leibowitz J.
    Journal: Symp Fundam Cancer Res; 1986; 38():97-111. PubMed ID: 3018882.
    Abstract:
    We have identified a recombinant leporipoxvirus that produces disseminated fibromas and a severe combined immune deficiency disease of sudden onset. The virus is recombinant between the SFV and the MV. MV was identified as a trace contaminant in stocks of SFV (Patuxent strain). Rabbits inoculated with the original uncloned stock of SFV prepared in vitro develop local tumors that subsequently regress. However, tumor extracts prepared from these animals, when injected into a second group of rabbits, produced MV syndrome. Rabbits with MV syndrome develop severe, usually lethal, Pasteurella or Bordetella infections and have disseminated fibroxanthosarcomas more similar to those produced by myxoma virus. The virus that induces this syndrome has been isolated by two cycles of plaque purification. This virus is indistinguishable from SFV using cross-neutralization and electron microscopy. Analyses of restriction enzyme digests of MV and plaque-purified SFV show them to be quite dissimilar and indicate that MV is recombinant between SFV and myxoma virus. This recombinational event resulted in approximately 5.5 kb of myxoma virus DNA within each of the inverted terminal repeats being replaced by a similar amount of DNA derived from the corresponding region of the SFV genome. Thus, MV contains approximately 149 kb of myxoma sequences and 11 kb of SFV sequences. Immunofluorescent studies of spleen and lymph nodes from MV-infected rabbits demonstrate that viral antigens are present predominantly in the sinusoidal lining cells in lymph nodes and in phagocytes in the splenic cords. This contrasts with the distribution of antigen observed in myxoma virus-infected rabbits where myxoma-specific antigens are present in large amounts in hyperplastic epithelium overlying tumors, particularly in the nasal mucosa and in spleen and lymph node cells. MV-infected rabbits essentially lose their lymphocyte proliferative response to T and B cell mitogens and are unable to initiate an antibody response to SRBC, as determined by a modified Jerne plaque assay. In vitro MV severely depresses the mitogen responses of normal B and T lymphocytes after two days of culture. Lymphoid cells and lysates of lymphoid cells from MV-infected rabbits will suppress mitogen- and antigen-induced responses in vitro. MV can grow in lymphocytes, but replication of MV is less efficient in lymphocytes than in RK-13 cells. Thus, MV produces a disseminated viral infection, systemic myxofibromas, and a severe combined immune deficiency in rabbits. The molecular and immunologic basis for these effects is now under study.
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