PubMed · 8766188
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C Grassi, S Spinaci. 1996. Why a TB corner?. https://pubmed.ncbi.nlm.nih.gov/8766188/
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Use of highly active antiretroviral treatment (HAART) has had a major impact on HIV-associated morbidity and mortality in industrialized countries. Access to HAART is now expanding in low-income countries where tuberculosis (TB) is the most important opportunistic disease. The incidence of TB has been fueled by the HIV epidemic and in many countries with high HIV prevalence current TB control measures are failing. HAART reduces the incidence of TB in treated cohorts by approximately 80% and therefore potentially has an important role in TB control in such countries. However, despite the huge beneficial effect of HAART, rates of TB among treated patients nevertheless remain persistently higher than among HIV-negative individuals. This observation raises the important question as to whether immune responses to Mycobacterium tuberculosis (MTB) are completely or only partially restored during HAART. Current data suggest that full restoration of circulating CD4 cell numbers occurs only among a minority of patients and that, even among these, phenotypic abnormalities and functional defects in lymphocyte subsets often persist. Suboptimal restoration of MTB-specific immune responses may greatly reduce the extent to which HAART is able to contribute to TB control at the community level because patients receiving HAART live much longer and yet would maintain a chronically heightened risk of TB.
OBJECTIVES: To assess whether highly active anti-retroviral therapy (HAART) contributes to the presentation of active tuberculosis (TB). DESIGN: Retrospective single-centre cohort study. METHODS: A total of 111 HIV-infected individuals with active TB were identified at an urban teaching hospital between February 1997 and April 2004. Those receiving HAART at the time of TB diagnosis were assessed. RESULTS: Nineteen of 111 (17%) were receiving HAART when TB developed. Within this group there appeared to be two distinct populations. Thirteen of 19, 12 from ethnic or social groups with high background rates of TB, developed disease a median of 41 days (range, 7-109) after starting HAART ('early TB' group). In six of 19 ('late TB' group), TB occurred a median of 358 days after HAART initiation (range, 258-598). The 'early TB' group had lower CD4 cell counts when starting HAART in comparison with the 'late TB' group (median; 87 versus 218 x 10 cells/l; P = 0.04); however no difference was observed in the rate of change of CD4 cell count (P = 0.5) or HIV load. Paradoxical reaction rate in the 'early TB' group was significantly greater than in the 'late-TB' group (62 versus 0%, P = 0.02) and greater than in a similar control population who started HAART while taking anti-TB therapy (62 versus 30%, P = 0.05). CONCLUSIONS: These data suggest anti-HIV treatment may amplify the presentation of active TB. This has implications for antiretroviral programmes in countries with high TB rates and warrants prospective investigation of a larger cohort.
Kaposi's sarcoma-associated herpesvirus (KSHV), the causative agent of Kaposi's sarcoma is able to infect several cell types. By investigating hyperplastic lymph nodes from AIDS patients with multicentric Castleman's disease, we demonstrate, for the first time, by dual colour immunohistochemistry, that KSHV is frequently detectable in germinal centre macrophages. These macrophages, which display a latency programme and frequently contain apoptotic bodies, may represent a non-negligible reservoir for the virus in lymphoid organs.