ArticleVirology journal2014
The dual role of tetraspanin CD63 in HIV-1 replication.
Article in Virology journal, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
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Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.
- Multiple Inhibitory Factors Act in the Late Phase of HIV-1 Replication: a Systematic Review of the Literature.Microbiology and molecular biology reviews : MMBR · 2018Pooled it
- Review
- Lipids, Tetraspanins, and Exosomes: Cell Factors inViruses · 2025Review
- Functional analysis ofThe Journal of general virology · 2025Article
- Extracellular vesicle isolation methods identify distinct HIV-1 particles released from chronically infected T-cells.Journal of extracellular vesicles · 2024Article
- Phospho-eIF4E stimulation regulates coronavirus entry by selective expression of cell membrane-residential factors.Journal of virology · 2024Article
- Antiviral HIV-1 SERINC restriction factors disrupt virus membrane asymmetry.Nature communications · 2023Article
- Lack of involvement of CD63 and CD9 tetraspanins in the extracellular vesicle content delivery process.Communications biology · 2023Article
- LAMP3/CD63 Expression in Early and Late Endosomes in Human Vaginal Epithelial Cells Is Associated with Enhancement of HSV-2 Infection.Journal of virology · 2022Article
- Rab3a, a small GTP-binding protein, is required for the stabilization of the murine leukaemia virus Gag protein.Small GTPases · 2022Article
- Tetraspanins: Host Factors in Viral Infections.International journal of molecular sciences · 2021Review
- HPV caught in the tetraspanin web?Medical microbiology and immunology · 2020Article
- Rapid Isolation of Rare Isotype-Switched Hybridoma Variants: Application to the Generation of IgG2a and IgG2b MAb to CD63, a Late Endosome and Exosome Marker.Antibodies (Basel, Switzerland) · 2020Article
- Intravenously delivered mesenchymal stem cell-derived exosomes target M2-type macrophages in the injured spinal cord.PloS one · 2018Article
- Tetraspanin Assemblies in Virus Infection.Frontiers in immunology · 2018Review
- Tetraspanins, Another Piece in the HIV-1 Replication Puzzle.Frontiers in immunology · 2018Review
- Proteomic Responses Under Cold Stress Reveal Unique Cold Tolerance Mechanisms in the Pacific White Shrimp (Frontiers in physiology · 2018Article
- Single-cell analysis identifies cellular markers of the HIV permissive cell.PLoS pathogens · 2017Article
- The Role of Exosomal VP40 in Ebola Virus Disease.DNA and cell biology · 2017Review
- Rab3a-Bound CD63 Is Degraded and Rab3a-Free CD63 Is Incorporated into HIV-1 Particles.Frontiers in microbiology · 2017Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundPreviously, we showed that the tetraspanin membrane protein CD63 mediates both early and post-integration stages of the HIV-1 replication cycle. The temporal roles of CD63 were discerned using monoclonal antibodies and small interfering RNAs (siRNAs) to block CD63 function, and determining which of the sequential steps in HIV-1 replication were disrupted. Inhibition was shown to occur during early infection, suggestive of involvement in virus entry or reverse transcription. In addition, we have shown that treatment with CD63 siRNA post-infection, significantly inhibited virus production in supernatant, suggesting an important role for CD63 in macrophages during HIV-1 replication events occurring after proviral integration, and possibly during egress.
resultsIn this study we used CD63 siRNA to investigate the infectivity of pseudotyped viruses (carrying an NL4-3 Env-negative luciferase backbone) in primary human macrophages. We demonstrated that lab adapted R5- and R5X4-tropic HIV-1 strains are significantly inhibited by CD63 silencing. However, the infectivity of MLV or VSV-pseudotyped strains, which enter though receptor-mediated endocytosis, is unaffected by silencing CD63. These results indicate that CD63 may support Env-mediated entry or fusion events facilitated though CD4 and CCR5. Also, antibody and siRNA-based CD63 inhibition studies indicate a potential role for CD63 following proviral integration. Further, we show that CD63 expression is key for efficient replication in primary CD4⁺ T cells, complementing our prior studies with primary human macrophages and immortalized cell lines.
conclusionsCollectively, these findings indicate that CD63 may support Env-mediated fusion as well as a late (post-integration) step in the HIV-1 replication cycle.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.