Invasive pneumococcal disease (PD) occurs frequently among HIV-infected patients, but it is unclear whether its manifestations and outcome are different compared to those observed among patients without HIV-1 infection. Because the immune reconstitution that accompanies antiretroviral therapy may change some of these features and because most cases of HIV- 1 infection occur in resource-poor settings of the world where access to antiretroviral agents is limited, we compared PD among patients with and without HIV-1 infection in a North American population before the introduction of highly active antiretroviral therapy (HAART). The records of all pneumococcal cultures processed at this medical center over a period of 20 months were used to identify patients with invasive PD.
View Article and Find Full Text PDFInterruption of all antiretroviral therapy for HIV-1 infection when therapy is failing and antiretroviral resistance has emerged is frequently associated with the disappearance of detectable resistance-associated protease and reverse transcriptase substitutions. However, the effect that discontinuation of treatment with a particular antiretroviral class has on resistance to that class when other antiretroviral therapy is continued is unknown. We investigated differences in detectable genotypic resistance to protease inhibitors (PI) and non-nucleoside reverse transcriptase inhibitors (NNRTI) among two populations: patients undergoing testing at the moment class-specific treatment failed (Group 1) and patients undergoing testing for varying periods after class-specific treatment failed and was discontinued but therapy with other antiretroviral classes continued with incomplete viral suppression (Group 2).
View Article and Find Full Text PDFGenotypic resistance to all antiretroviral classes was widespread among human immunodeficiency virus type 1 isolates failing therapy. Resistance to nonnucleoside reverse transcriptase inhibitors was found most frequently and resistance to protease inhibitors was found least frequently, most likely due to differences in the number of enzymatic amino acid substitutions leading to resistance to each particular drug class.
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