ArticleRetrovirology2020
M-Sec facilitates intercellular transmission of HIV-1 through multiple mechanisms.
Article in Retrovirology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.
- Mitochondrial Transfer in the Neurovascular Unit, Not Only for Energy Rescue: A Systematic Review.Aging and disease · 2024Pooled it
- Three immunoregulatory signatures define non-productive HIV infection in stem cell memory CD4Nature communications · 2026Article
- Tunneling nanotubes: a new dimension of intercellular communication and recent progress.Cell communication and signaling : CCS · 2026Review
- Mitochondrial Transport in Bone Metabolism Homeostasis: Molecular Mechanisms and Targeted Therapeutic Strategies.International journal of molecular sciences · 2026Review
- M-Sec promotes the production of infectious HIV-1 virus through the exocyst complex in macrophages.PLoS pathogens · 2026Article
- Glycolysis inhibition in tuberculosis-driven metabolic rewiring reduces HIV-1 spread in macrophages.Life science alliance · 2026Article
- Breaking cellular boundaries: molecular mechanisms of tunneling nanotube formation and fusion.Biochemical Society transactions · 2026Review
- Three immunoregulatory signatures define non-productive HIV infection in CD4bioRxiv : the preprint server for biology · 2026Article
- The role of mitochondrial transfer in lung disease.Respiratory research · 2025Review
- Intercellular highways of viral spread: tunneling nanotubes and extracellular vesicles at the maternal-fetal interface.Current opinion in virology · 2025Review
- Identification of TNFAIP2 as a unique cellular regulator of CSF-1 receptor activation.Life science alliance · 2025Article
- M-Sec promotes the accumulation of intracellular HTLV-1 Gag puncta and the incorporation of Env into viral particles.PLoS pathogens · 2025Article
- Horizontal mitochondrial transfer as a novel bioenergetic tool for mesenchymal stromal/stem cells: molecular mechanisms and therapeutic potential in a variety of diseases.Journal of translational medicine · 2024Review
- Role of Monocyte/Macrophages in the Pathogenesis of NeuroHIV.Results and problems in cell differentiation · 2024Review
- A role for tunneling nanotubes in virus spread.Frontiers in microbiology · 2024Review
- The role of tunneling nanotubes during early stages of HIV infection and reactivation: implications in HIV cure.NeuroImmune pharmacology and therapeutics · 2023Review
- Non-Classical Intercellular Communications: Basic Mechanisms and Roles in Biology and Medicine.International journal of molecular sciences · 2023Review
- Mitochondrial transplantation: opportunities and challenges in the treatment of obesity, diabetes, and nonalcoholic fatty liver disease.Journal of translational medicine · 2022Review
- HIV-1Biomolecules · 2022Article
- Miro proteins and their role in mitochondrial transfer in cancer and beyond.Frontiers in cell and developmental biology · 2022Review
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHIV-1 promotes the formation of tunneling nanotubes (TNTs) that connect distant cells, aiding cell-to-cell viral transmission between macrophages. Our recent study suggests that the cellular protein M-Sec plays a role in these processes. However, the timing, mechanism, and to what extent M-Sec contributes to HIV-1 transmission is not fully understood, and the lack of a cell line model that mimics macrophages has hindered in-depth analysis.
resultsWe found that HIV-1 increased the number, length and thickness of TNTs in a manner dependent on its pathogenic protein Nef and M-Sec in U87 cells, as observed in macrophages. In addition, we found that M-Sec was required not only for TNT formation but also motility of U87 cells, both of which are beneficial for viral transmission. In fact, M-Sec knockdown in U87 cells led to a significantly delayed viral production in both cellular and extracellular fractions. This inhibition was observed for wild-type virus, but not for a mutant virus lacking Nef, which is known to promote not only TNT formation but also migration of infected macrophages.
conclusionsBy taking advantage of useful features of U87 cells, we provided evidence that M-Sec mediates a rapid and efficient cell-cell transmission of HIV-1 at an early phase of infection by enhancing both TNT formation and cell motility.
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