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Introduction: Tat protein is a trans-activator of HIV-1 genome transcription, with additional functions including the ability to induce the chronic inflammatory process. Natural amino acid polymorphisms in Tat may affect its functional properties and the course of HIV infection. The aim of this work is to analyze the marks of Tat consensus sequences in non-A6 HIV-1 variants characteristic of the Russian Federation, as well as study natural polymorphisms in Tat CRF63_02A6 and subtype B variants circulating in Russia.
View Article and Find Full Text PDFDevelopment of a latency model for HIV-1 subtype C and the impact of long terminal repeat element genetic variation on latency reversal.
J Virus Erad
December 2024
HIV Pathogenesis Programme, The Doris Duke Medical Research Institute, Nelson R. Mandela School of Medicine, University of KwaZulu-Natal, Durban, South Africa.
Sub-Saharan Africa accounts for almost 70 % of people living with HIV (PLWH) worldwide, with the greatest numbers centred in South Africa where 98 % of infections are caused by subtype C (HIV-1C). However, HIV-1 subtype B (HIV-1B), prevalent in Europe and North America, has been the focus of most cure research and testing despite making up only 12 % of HIV-1 infections globally. Development of latency models for non-subtype B viruses is a necessary step to address this disproportionate focus.
View Article and Find Full Text PDFSex Affects Cognitive Outcomes in HIV-1 Tat Transgenic Mice: Role of CCR5.
ASN Neuro
January 2025
Department of Anatomy and Neurobiology, Virginia Commonwealth University, Richmond, Virginia, USA.
People living with HIV (PLWH) experience HIV-associated neurocognitive disorders (HAND), even though combination antiretroviral therapy (cART) suppresses HIV replication. HIV-1 transactivator of transcription (HIV-1 Tat) contributes to the development of HAND through neuroinflammatory and neurotoxic mechanisms. C-C chemokine 5 receptor (CCR5) is important in immune cell targeting and is a co-receptor for HIV viral entry into CD4+ cells.
View Article and Find Full Text PDFInflammatory Monocytes Increase Prior to Detectable HIV-1 Rebound Viremia.
bioRxiv
December 2024
Fred Hutchinson Cancer Center, Vaccine and Infectious Disease Division, Seattle, WA 98109.
The persistence of HIV-1 proviruses in latently infected cells allows viremia to resume upon treatment cessation. To characterize the resulting immune response, we compare plasma proteomics and single-cell transcriptomics of peripheral blood mononuclear cells (PBMCs) before, during, and after detectable plasma viremia. We observe unique transcriptional signatures prior to viral rebound including a significant increase in CD16 monocytes with increased anti-viral gene expression.
View Article and Find Full Text PDFGenetic Characterization of HIV-1 Gene from Virologically Controlled Aging Individuals with HIV on Long-Term Antiretroviral Therapy.
AIDS Res Hum Retroviruses
December 2024
Department of Immunobiology, College of Medicine, University of Arizona, Tucson, Arizona, USA.
Despite advancements in antiretroviral therapy (ART) that reduces the viral load to undetectable levels and improve CD4 T cell counts, viral eradication has not been achieved due to HIV-1 persistence in resting CD4 T-cells. We, therefore, characterized the gene, which is essential for HIV-1 replication and pathogenesis, from 20 virologically controlled aging individuals with HIV (HIV) on long-term ART and improved CD4 T-cell counts, with a particular focus on older individuals. Peripheral blood mononuclear cell genomic DNA from HIV were used to amplify gene by polymerase chain reaction followed by nucleotide sequencing and analysis.
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