Last year, we reported that seven of eight rhesus monkeys (RM) coinfected with Mycobacterium leprae (ML) and simian immunodeficiency virus (SIV, 8-10 months pre-ML) harbored acid-fast bacilli (AFB) at sites of dermal inoculation and/or at disseminated sites (nasal mucosa) at times of humane sacrifice (up to 270 days post-ML inoculation) due to SIV-induced debilitation or, in one long- term survivor's case, to date over 3 years post-ML inoculation. Detectable AFB were cleared in biopsies of inoculation sites of RM inoculated with ML alone after 63 days postinoculation; these sites have, so far, remained AFB-negative, thereafter. Compared to animals infected with ML alone, RM coinfected with SIV plus ML showed 1) completely suppressed serum antibody responses to ML-specific phenolic-glycolipid-I and to mycobacteria-common lipoarabinomannan antigens, but strong anti-SIV Gp120 antibody responses; 2) impaired sensitization of blood mononuclear cells (MNC) to in vitro recognition of ML-specific antigens in blastogenic stimulation assays; 3) impaired in vitro responses of blood MNC to nonspecific (ConA) blastogenic stimuli and 4) early post-ML inoculation, there was a significant incremental diminution of percentages of blood CD4+CD29+ T-cells in addition to the existing SIV-induced diminished percentages of the CD4+CD29+ subpopulation. A follow-up study last year in groups of 6 RM that is still in progress showed that SIV given at the same time as ML is significantly more lethal than SIV inoculated 2 weeks prior to ML; both of these inoculation procedures are effective in inducing increased susceptibility to leprosy. The immunologic conclusions described above were confirmed in this follow-up, but differences in relative timing of inoculation with the 2 agents result in differing degrees of modification in immune responses to ML antigens. The results indicate that humoral and cellular immune responses to ML antigens are compromised in ML-inoculated RM that are coinfected with SIV and provide an immunologic basis for our demonstration of enhanced ML persistence or leprosy susceptibility in SIV-ML coinfected RM. The data also provide a probable explanation for the inconsistent observation of increased leprosy risk in HIV-positive patients in the field. It is believed that many of the visible (dermal) symptoms of leprosy are the result of the immune response to ML antigens. Since the immunologic response to ML antigens is compromised in AIDS virus-coinfected patients, it is reasonable to assume that leprosy symptoms would be less obvious, on the average, in coinfected patients. Thus, many coinfected patients would be selectively excluded from field studies that depend upon leprosy recognition followed by secondary, correlational studies for virus infection. Such studies would be expected to erroneously conclude
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