ArticleVirology2007
Loss of the N-linked glycosylation site at position 386 in the HIV envelope V4 region enhances macrophage tropism and is associated with dementia.
Article in Virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
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Who cites it
65 citing papers in PubMed, 89 citations in OpenAlex.
- Characterization of HIV variants from paired Cerebrospinal fluid and Plasma samples in primary microglia and CD4Journal of neurovirology · 2024Article
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- SHIV-C109p5 NHP induces rapid disease progression in elderly macaques with extensive GI viral replication.Journal of virology · 2024Article
- HIV-1CViruses · 2020Article
- A minor population of macrophage-tropic HIV-1 variants is identified in recrudescing viremia following analytic treatment interruption.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- CCR5 structural plasticity shapes HIV-1 phenotypic properties.PLoS pathogens · 2018Article
- Structural Rearrangements Maintain the Glycan Shield of an HIV-1 Envelope Trimer After the Loss of a Glycan.Scientific reports · 2018Article
- Ultradeep single-molecule real-time sequencing of HIV envelope reveals complete compartmentalization of highly macrophage-tropic R5 proviral variants in brain and CXCR4-using variants in immune and peripheral tissues.Journal of neurovirology · 2018Article
- Molecular Signatures of HIV-1 Envelope Associated with HIV-Associated Neurocognitive Disorders.Current HIV/AIDS reports · 2018Review
- Identification of Emerging Macrophage-Tropic HIV-1 R5 Variants in Brain Tissue of AIDS Patients without Severe Neurological Complications.Journal of virology · 2017Article
- Delineating CD4 dependency of HIV-1: Adaptation to infect low level CD4 expressing target cells widens cellular tropism but severely impacts on envelope functionality.PLoS pathogens · 2017Article
- Tissue-resident macrophages can contain replication-competent virus in antiretroviral-naive, SIV-infected Asian macaques.JCI insight · 2017Article
- Immune Responses in the Central Nervous System Are Anatomically Segregated in a Non-Human Primate Model of Human Immunodeficiency Virus Infection.Frontiers in immunology · 2017Article
- Phenotypic Correlates of HIV-1 Macrophage Tropism.Journal of virology · 2015Article
- Envelope gene evolution and HIV-1 neuropathogenesis.Journal of neuroinfectious diseases · 2015Article
- Article
- Compartmentalization, Viral Evolution, and Viral Latency of HIV in the CNS.Current HIV/AIDS reports · 2015Review
- HIV-1 target cells in the CNS.Journal of neurovirology · 2015Review
- HIV-1 non-macrophage-tropic R5 envelope glycoproteins are not more tropic for entry into primary CD4+ T-cells than envelopes highly adapted for macrophages.Retrovirology · 2015Article
- Single genome analysis reveals genetic characteristics of Neuroadaptation across HIV-1 envelope.Retrovirology · 2014Article
5 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
HIV infects macrophages and microglia in the central nervous system (CNS). Mechanisms that enhance HIV macrophage/microglial tropism are not well understood. Here, we identify an HIV Env variant in the V4 region of gp120, Asp 386 (D386), that eliminates an N-linked glycosylation site at position 386, enhances viral replication in macrophages, and is present at a higher frequency in AIDS patients with HIV-associated dementia (HAD) compared with non-HAD patients. D386 enhances HIV entry and replication in macrophages but not in microglia or peripheral blood mononuclear cells, possibly due to differential glycosylation in these cell types. A D386N mutation in the UK1br Env, which restores the N-linked glycan site, reduced neutralization sensitivity to the IgG1b12 (b12) monoclonal antibody, which recognizes a conserved neutralization epitope that overlaps the CD4 binding site. Molecular modeling suggested that loss of the glycan at position 386 increases exposure of the CD4 and b12 binding sites on gp120. Loss of a glycan at 386 was more frequent in Envs from HAD patients (26%; n=185) compared with non-HAD patients (7%; n=99; p<0.001). The most significant association of these Env variants with HAD was in blood or lymphoid tissue rather than brain. These findings suggest that increased exposure of the b12 epitope overlapping the CD4 binding site via elimination of a glycan at position 386 is associated with enhanced HIV macrophage tropism, and provide evidence that determinants of macrophage and microglia tropism are overlapping but distinct.
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