Document 0195
 DOCN  M9440195
 TI    Murine AIDS is initiated in the lymph nodes draining the site of
       inoculation, and the infected B cells influence T cells located at
       distance, in noninfected organs.
 DT    9404
 AU    Simard C; Huang M; Jolicoeur P; Laboratory of Molecular Biology,
       Clinical Research Institute of; Montreal, Quebec, Canada.
 SO    J Virol. 1994 Mar;68(3):1903-12. Unique Identifier : AIDSLINE
       MED/94149885
 AB    The infection of cells which belong to the B-cell lineage is thought to
       be the primary event leading to the phenotypic and functional
       alterations seen in the murine AIDS (M. Huang, C. Simard, D. Kay, and P.
       Jolicoeur, J. Virol. 65:6562-6571, 1991). Using in situ hybridization,
       we studied the time course of the anatomic distribution of the murine
       AIDS-infected B cells in C57BL/6 mice inoculated intraperitoneally or in
       the foot pad with helper-free stocks of the defective murine AIDS virus.
       The local lymph nodes draining the injection site (the mediastinal or
       popliteal lymph nodes) were the primary organs in which infected B cells
       could be detected. From this initial site, the proliferating infected B
       cells were found to migrate progressively to most of the other lymph
       nodes and to the spleen. The bone marrow cells (containing the precursor
       B cells) were not found to be infected by the virus. These results
       suggest that the defective murine AIDS virus infects mature Ly-1- B
       cells present in lymph nodes. We compared the concanavalin A response of
       the T cells at an early time postinoculation, before all lymphoid organs
       are infiltrated with infected B cells. In lymphoid organs free of
       infected B cells, T cells were found to be hyperresponsive. In lymphoid
       organs in which infected B cells were present, T cells were
       hyporesponsive. These data suggest that infected B cells influence
       distant T cells, maybe by the release of a circulating factor or through
       another uninfected cell population activated by the infected B cells.
 DE    Animal  B-Lymphocytes/*MICROBIOLOGY  Bone Marrow/MICROBIOLOGY  *Cell
       Communication  Concanavalin A/PHARMACOLOGY  Defective Viruses  Flow
       Cytometry  In Situ Hybridization  Lymph Nodes/*MICROBIOLOGY  Mice  Mice,
       Inbred C57BL  Murine Acquired Immunodeficiency Syndrome/*IMMUNOLOGY/
       *MICROBIOLOGY  Retroviridae/GROWTH & DEVELOPMENT/GENETICS  Support,
       Non-U.S. Gov't  T-Lymphocytes/DRUG EFFECTS/*IMMUNOLOGY  Time Factors
       Tissue Distribution  JOURNAL ARTICLE

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