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Huge research effort has been invested over many years to determine the phenotypes of natural or artificial mutations in HIV proteins--interpretation of mutation phenotypes is an invaluable source of new knowledge. The results of this research effort are recorded in the scientific literature, but it is difficult for virologists to rapidly find it. Manually locating data on phenotypic variation within the approximately 270,000 available HIV-related research articles, or the further 1,500 articles that are published each month is a daunting task. Accordingly, the HIV research community would benefit from a resource cataloguing the available HIV mutation literature. We have applied computational text-mining techniques to parse and map mutagenesis and polymorphism information from the HIV literature, have enriched the data with ancillary information and have developed a public, web-based interface through which it can be intuitively explored: the HIV mutation browser. The current release of the HIV mutation browser describes the phenotypes of 7,608 unique mutations at 2,520 sites in the HIV proteome, resulting from the analysis of 120,899 papers. The mutation information for each protein is organised in a residue-centric manner and each residue is linked to the relevant experimental literature. The importance of HIV as a global health burden advocates extensive effort to maximise the efficiency of HIV research. The HIV mutation browser provides a valuable new resource for the research community. The HIV mutation browser is available at: http://hivmut.org.
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http://dx.doi.org/10.1371/journal.pcbi.1003951 | DOI Listing |
mBio
September 2025
Centre de Recherche du CHUM, Montreal, Québec, Canada.
HIV-1-mediated CD4 downregulation is a well-known mechanism that protects infected cells from antibody-dependent cellular cytotoxicity (ADCC). While CD4 downregulation by HIV-1 Nef and Vpu proteins has been extensively studied, the contribution of the HIV-1 envelope glycoprotein (Env) in this mechanism is less understood. While Env is known to retain CD4 in the endoplasmic reticulum (ER) through its CD4-binding site (CD4bs), little is known about the mechanisms underlying this process.
View Article and Find Full Text PDFFront Microbiol
August 2025
Institute of Infectious Diseases, Guangzhou Eighth People's Hospital, Guangzhou Medical University, Guangzhou, Guangdong, China.
Introduction: Low-level viremia (LLV) in HIV infection, defined as detectable but low plasma viral load, is associated with an increased risk of virological failure (VF); however, the mechanisms underlying LLV remain unclear. Monocytes, as potential viral reservoirs, can migrate into tissues and differentiate into tissue-resident macrophage reservoirs, playing a critical role in viral dissemination and potentially driving persistent viremia.
Methods: This study aimed to analyze and compare the molecular characteristics of near-full-length HIV-1 proviral DNA quasispecies from monocytes in three distinct virological response groups: VF, LLV, and virological suppression (VS).
HIV Med
September 2025
Department of Medical Microbiology, Faculty of Medicine, Hacettepe University, Ankara, Türkiye.
Introduction: Monitoring transmitted drug resistance is crucial for guiding first-line antiretroviral therapy (ART) and controlling the rising HIV epidemic in Türkiye. This study aimed to determine the prevalence of transmitted antiretroviral resistance to protease inhibitors (PIs), nucleoside reverse transcriptase inhibitors (NRTIs), non-nucleoside reverse transcriptase inhibitors (NNRTIs), integrase strand transfer inhibitors (INSTIs) and capsid assembly inhibitors (CAIs). We also assessed the distribution of HIV-1 subtypes and circulating recombinant forms (CRFs) at one of the main national referral centres in Türkiye.
View Article and Find Full Text PDFJ Autoimmun
September 2025
Garvan Institute of Medical Research, Darlinghurst, NSW, Australia; Cellular Genomics Futures Institute & School of Biomedical Sciences, UNSW Sydney, Australia. Electronic address:
Background: In autoimmune disease it is not understood how self-reactive B cells escape immune tolerance checkpoints to produce pathogenic autoantibodies.
Objective: In patients with demyelinating polyneuropathy caused by IgM autoantibodies against myelin associated glycoprotein (MAG) and the sulphated trisaccharide CD57, we aimed to test the hypothesis that B cells making the autoantibody escaped tolerance by acquiring lymphoma driver somatic mutations.
Methods: Deep single-cell RNA, DNA, flow cytometric and antibody specificity analysis of blood from three patients with MAG neuropathy.
J Virol
September 2025
Division of Medical Virology, Institute of Infectious Disease and Molecular Medicine, University of Cape Town, Cape Town, South Africa.
Unlabelled: Ongoing viral evolution in immunocompromised individuals with persistent infection may facilitate the evolution of SARS-CoV-2 and emergence of variants of concern (VOC). This study was conducted in the Western Cape Province of South Africa where the HIV prevalence is around 8%, with limited information on the frequency of persistent SARS-CoV-2 infection, the pattern of evolution in these individuals, and if these variants contribute to the diversity of circulating viruses. This study investigated 75 individuals with two or more SARS-CoV-2 diagnoses at least one month apart.
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