Abrogation of resistance to severe mousepox in C57BL/6 mice infected with LP-BM5 murine leukemia viruses.
Strain C57BL/6 (B6) mice infected with LP-BM5 murine leukemia virus (MuLV) develop a disease which combines abnormal lymphoproliferation with profound immunosuppression and has many features in common with human acquired immunodeficiency syndrome induced by HTLV-III/LAV retroviruses. To determine whether this LP-BM5 MuLV infection would affect the innate resistance of B6 mice to a naturally occurring, highly virulent murine pathogen, mice were exposed to ectromelia virus at various times after treatment with LP-BM5 viruses. At week 4 after infection with LP-BM5, mice challenged with ectromelia virus were unable to generate a humoral immune response to this virus, and between weeks 8 and 10 after infection, challenged mice lost the ability to generate an ectromelia virus-specific cytotoxic-T-cell response. Loss of the cellular immune responses to ectromelia virus was associated with an increased susceptibility to the lethal effects of the virus.
D000818:Animals; D002460:Cell Line; D004481:Ectromelia virus / Q000276:immunology*; D004482:Ectromelia, Infectious / Q000276:immunology*; D005260:Female; D007113:Immunity, Innate; D009052:Leukemia Virus, Murine / Q000276:immunology*; D007942:Leukemia, Experimental / Q000276:immunology*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D011213:Poxviridae Infections / Q000276:immunology*; D010948:Viral Plaque Assay