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Publication : Effect of non-H-2-linked genes on anti-virus immune responses and long-term survival in mice persistently infected with E-55+ murine leukemia virus.

First Author  Avidan N Year  1995
Journal  Virology Volume  211
Issue  2 Pages  507-15
PubMed ID  7645254 Mgi Jnum  J:28300
Mgi Id  MGI:75921 Doi  10.1006/viro.1995.1432
Citation  Avidan N, et al. (1995) Effect of non-H-2-linked genes on anti-virus immune responses and long-term survival in mice persistently infected with E-55+ murine leukemia virus. Virology 211(2):507-15
abstractText  We have previously demonstrated that BALB/c-H-2k (BALB.K) mice are susceptible to the development of thymic lymphoma induced by E-55+ murine leukemia virus (MuLV). In the present studies, C57BL/10-H-2k (B10.BR) mice were found to be resistant to E-55+ MuLV-induced lymphoma despite the fact that these mice become persistently infected. This resistance to lymphomagensis is mediated by the anti-virus immune response since immunosuppressed mice progress to develop disease. The protective immune response in B10.BR mice is bimodal with respect to time after virus infection. The early immune response results in a dramatic decrease in the number of virus-infected cells within 4-8 weeks after infection. This decrease in virus-infected cells occurs in immunocompetent mice from strains that are either resistant (B10.BR) or susceptible (BALB.K) to E-55+ MuLV-induced disease. Subsequently, susceptible mice develop an increase in infected cells, whereas no increase in infected cells occurs in resistant mice despite the fact that they are persistently infected. This later phase of resistance in B10.BR appears to be mediated by T cells. Since B10.BR and BALB.K both express the H-2k haplotype, resistance appears to be mediated by a non-H-2-linked gene(s). (BALB.K x B10.BR)F1 mice are resistant to disease development, indicating resistance is a dominant trait.
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