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Deals with a study which described the evolution of infections in a group of HIV-infected patients with latent visceral leishmaniasis (VL) who received antiretroviral therapy after VL was diagnosed. Background on the introduction of highly active antiretroviral therapy; Methodology; Results and discussion.

Persistent cytomegalovirus (CMV) infection has been suggested to be a major driving force in the immune deterioration and an underlying source of age-related diseases in the elderly. CMV antibody titers are associated with lower responses to vaccination, cardiovascular diseases, frailty, and mortality. CMV infection is also associated with shorter T-cell telomeres and replicative senescence. Although an age-related deregulation of CMV-specific T-cell responses could be an underlying cause of the relationship between CMV and immune defects, strong and polyfunctional responses are observed in elderly individuals, casting uncertainty on their direct role in age-related immune frailty. In this study, we longitudinally followed a cohort of healthy donors aged over 50 years, assessing their mortality rates and time to death during a 2-year period. Specific T-cell responses to the immunodominant antigen pp65 (IFNγ, TNFα, IL2, MIP1α, CD107a, and perforin production) were analyzed at the beginning of the 2-year observation period. A cytotoxic CD8 pp65-specific T-cell response, without cytokine or chemokine coexpression, was independently associated with all-cause mortality in these elderly individuals. This pp65-specific CD8 T-cell response could be a useful tool to identify individuals with depressed immune function and a higher risk of death. [ABSTRACT FROM AUTHOR]

Genotyping of human immunodeficiency virus type 1 (HIV-1) for antiretroviral drug resistance is routinely used both in clinical practice, to guide the selection of options for an individual's antiretroviral therapy, and in epidemiological studies, to estimate levels of antiretroviral drug resistance in a patient population. However, reliance on results of a single test can result in an underestimation of antiretroviral drug resistance. In the present study, we quantified the prevalence of resistance-associated mutations found in recent genotypic tests of 1734 HIV-1-infected, treatment-experienced subjects who had at least 3 genotypic tests ( genotypic np11,404 tests total; median, 5 tests/subject) and compared it with that of resistance-associated mutations ever detected in these subjects between 1996 and 2004. Single-point analyses underestimated antiretroviral drug resistance, particularly for nucleoside analogues, in both individuals and patient populations. For example, the prevalence of resistance-associated mutation M184V/I was 25.5% in the most recent genotypes and 58.8% in available historical genotypes. Our results suggest that analysis of a combined historical genotype rather than of a crosssectional genotype may lead to more accurate estimates of antiretroviral drug resistance in individual patients and in patient populations. [ABSTRACT FROM AUTHOR]

Thymic function was evaluated in 32 heavily antiretroviral-treated human immunodeficiency virus type 1 (HIV-1)-infected adults with long-term virologic treatment failure by measuring thymic volume, by determining the absolute number of naive T cell phenotypes, and by determining the number of cells carrying T cell receptor excision circles (TRECs). There was a significant inverse correlation between age and thymic volume (r = -0.415; P = .018), and there was a significant direct correlation between thymic volume and total naive T cell counts (r = 0.529; P = .002), naive CD4[sup +] cell counts (r = 0.437; P = .012), naive CD8[sup +] cell counts (r = 0.467; P = .007), and TREC levels (r = 0.391; P = .027). In conclusion, this study found clear evidence that the thymus of heavily antiretroviral-treated HIV-l-infected adults with long-term virologic treatment failure is actively engaged in thymopoiesis, which generates new naive T cells for the peripheral lymphocyte pool. [ABSTRACT FROM AUTHOR]