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Variability in HIV-1 transmitted/founder virus susceptibility to combined APOBEC3F and APOBEC3G host restriction.
J Virol
December 2024
Department of Biochemistry, Microbiology, and Immunology, College of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada.
Several APOBEC3 enzymes restrict HIV-1 by deaminating cytosine to form uracil in single-stranded proviral (-)DNA. However, HIV-1 Vif counteracts their activity by inducing their proteasomal degradation. This counteraction by Vif is incomplete, as evidenced by footprints of APOBEC3-mediated mutations within integrated proviral genomes of people living with HIV-1.
View Article and Find Full Text PDFGut microbiota profiling in injection drug users with and without HIV-1 infection in Puerto Rico.
Front Microbiol
November 2024
Department of Animal Science, University of Nebraska-Lincoln, Lincoln, NE, United States.
Introduction: The full extent of interactions between human immunodeficiency virus (HIV) infection, injection drug use, and the human microbiome is unclear. In this study, we examined the microbiomes of HIV-positive and HIV-negative individuals, both drug-injecting and non-injecting, to identify bacterial community changes in response to HIV and drug use. We utilized a well-established cohort of people who inject drugs in Puerto Rico, a region with historically high levels of injection drug use and an HIV incidence rate disproportionately associated with drug use.
View Article and Find Full Text PDFNeuropathy among drug resistant HIV Patients treated in Jakarta.
J Infect Dev Ctries
November 2024
Department of Microbiology, Faculty of Medicine, Universitas Indonesia, Jakarta, Indonesia.
Introduction: Some people living with HIV (PLWH) receiving ART in Indonesia display poor clearance of replicating virus. This has been associated with HIV-associated sensory neuropathy. Here we assess whether treatment failure reflects the presence of drug resistance mutations.
View Article and Find Full Text PDFDisruption of LEDGF/p75-directed integration derepresses antisense transcription of the HIV-1 genome.
bioRxiv
December 2024
Center for ViroScience and Cure, Laboratory of Biochemical Pharmacology, Department of Pediatrics, Emory University School of Medicine; Atlanta, GA, USA.
Disruption of HIV-1 Integrase (IN) interactions with the host-factor Lens Epithelium-Derived Growth Factor (LEDGF)/p75 leads to decreased, random integration, increased latent infection, and described here, accumulation of HIV-1 antisense RNA (asRNA). asRNA increase was observed following interruptions of IN-LEDGF/p75 interactions either through pharmacologic perturbations of IN-LEDGF/p75 by treatment with allosteric HIV-1 integrase inhibitors (ALLINIs) or in cell lines with LEDGF genetic knockout. Additionally, by impairing Tat-dependent HIV transcription, asRNA abundance markedly increases.
View Article and Find Full Text PDFAntiretroviral therapy (ART) controls HIV-1 replication in people with HIV-1 (PWH), but immunological restauration at mucosal barrier surfaces is not achieved. This fuels microbial translocation, chronic immune activation, and increased comorbidities, including cardiovascular disease (CVD). Here, we sought to identify novel markers of mucosal barrier impairment in the blood to predict the HIV and/or CVD status.
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