Mycobacterium avium complex (MAC) is a common opportunistic infection in human AIDS patients resulting from a unique synergy between HIV and mycobacterial organisms. SIV-infected macaques also develop MAC in the terminal stages of disease sharing features with the condition in human patients. We have shown an association between the occurrence of MAC and specific strains of SIV suggesting that viral determinants play a critical and specific role in disease pathogenesis. To begin to investigate this unique synergy between SIV and MAC a morphologic study was undertaken comparing MAC infected and uninfected mesenteric lymph nodes from SIV-inoculated macaques. Concurrent infection of macrophages with SIV and MAC as detected by in situ hybridization or in situ PCR for viral nucleic acid and Ziehl-Neelsen acid fast stain for bacterial organisms was not detected. Progressive effacement of mesenteric lymph node by MAC infected macrophages was associated with decreased numbers of CD4 positive lymphocytes, infiltration by CD8 positive lymphocytes, formation of perivascular B cell aggregates and increased localization of TGF- . Furthermore with increasing mycobacterial load there is decreased expression of CD4, HLA-DR and CD14 by infected macrophages. Decreased recruitment of CD4 positive lymphocytes occurred despite increased expression of VCAM-1 and ICAM-1 by lymph node vascular endothelium and continued recruitment of these cells to other inflammatory sites within the same animal. Our results indicate that alterations in lymphocyte subsets and cytokine and adhesion molecule expression occur concurrently with and do not precede dissemination of mycobacterial infection. Moreover, in vivo mycobacterial infection of macrophages is associated with decreased expression of functional cell surface markers and suggest strategies employed by this pathogen to evade the host immune response. Currently we are utilizing a RAPD PCR technique to investigate the molecular epidemiology of MAC infection in our colony and
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