Studies of the susceptibility of nude, CD4 knockout, and SCID mutant mice to the disease induced by the murine AIDS defective virus.
Murine AIDS (MAIDS) is induced by a defective retrovirus that infects lymphocyte cells of the B lineage. To determine whether functional T cells are required for the infection of B cells, T-cell-deficient mice (nude, CD4 knockout, and SCII)) were infected with helper-free stocks of the MAIDS defective virus. Infection of B cells was monitored by Northern blot analysis and in situ hybridization. The C57BL/6 nude mice contained clusters of infected B cells, but less so than did the euthymic mice. In contrast, the (C57BL/6 x BALB/c)F1 nude mice harbored more infected B cells than did their euthymic littermates when maintained in a pathogen-free environment. Clusters of infected B cells were also detected in the MAIDS virus-infected CD4-/- knockout mice despite the total absence of CD4+ T cells in these mice. However, infected cells were not detected in SCID mice (deficient in mature T and B cells) inoculated with the same virus, indicating that precursor B cells are not a target of the virus in the absence of mature CD4+ T cells. These data confirm that the primary event in the development of MAIDS is the infection of relatively mature peripheral B cells and that CD4+ T cells are required to promote the expansion of these infected B cells.
Simard
C
C
Laboratory of Molecular Biology, Clinical Research Institute of Montreal, Quebec, Canada.
Klein
S J
SJ
Mak
T
T
Jolicoeur
P
P
D000818:Animals; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology*; D003673:Defective Viruses / Q000276:immunology*; D004198:Disease Susceptibility / Q000276:immunology; D005260:Female; D007113:Immunity, Innate / Q000276:immunology; D009052:Leukemia Virus, Murine / Q000276:immunology*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D008819:Mice, Nude; D016513:Mice, SCID; D016183:Murine Acquired Immunodeficiency Syndrome / Q000276:immunology* / Q000821:virology