ArticlemBio2019
Potent Enhancement of HIV-1 Replication by Nef in the Absence of SERINC3 and SERINC5.
Article in mBio, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
22 citing papers in PubMed, 33 citations in OpenAlex.
- Restriction of HIV-1 infectivity by interferon and IFITM3 is counteracted by Nef.Science advances · 2025Article
- The ectodomain sheddase ADAM10 restricts HIV-1 propagation and is counteracted by Nef.Science advances · 2025Article
- Genetic determinants of HIV-1 subtype C Nef-mediated SERINC3 down-regulation.Virology journal · 2025Article
- Replication competent HIV-guided CRISPR screen identifies antiviral factors including targets of the accessory protein Nef.Nature communications · 2024Article
- Beyond Impairment of Virion Infectivity: New Activities of the Anti-HIV Host Cell Factor SERINC5.Viruses · 2024Review
- Interactions between HIV proteins and host restriction factors: implications for potential therapeutic intervention in HIV infection.Frontiers in immunology · 2024Review
- HIV-1 subtype C Nef-mediated SERINC5 down-regulation significantly contributes to overall Nef activity.Retrovirology · 2023Article
- Article
- Nef enhances HIV-1 replication and infectivity independently of SERINC5 in CEM T cells.Virology · 2023Article
- HIV-1 propagation is highly dependent on basal levels of the restriction factor BST2.Science advances · 2021Article
- Aromatic Side Chain at Position 412 of SERINC5 Exerts Restriction Activity toward HIV-1 and Other Retroviruses.Journal of virology · 2021Article
- SERINC5 Can Enhance Proinflammatory Cytokine Production by Primary Human Myeloid Cells in Response to Challenge with HIV-1 Particles.Journal of virology · 2021Article
- Selective Disruption of SERINC5 Antagonism by Nef Impairs SIV Replication in Primary CD4Journal of virology · 2021Article
- Nef homodimers down-regulate SERINC5 by AP-2-mediated endocytosis to promote HIV-1 infectivity.The Journal of biological chemistry · 2020Article
- Variation in HIV-1 Nef function within and among viral subtypes reveals genetically separable antagonism of SERINC3 and SERINC5.PLoS pathogens · 2020Article
- HIV-1 Nef dimers short-circuit immune receptor signaling by activating Tec-family kinases at the host cell membrane.The Journal of biological chemistry · 2020Article
- Loss of tetherin antagonism by Nef impairs SIV replication during acute infection of rhesus macaques.PLoS pathogens · 2020Article
- SERINC5 Inhibits the Secretion of Complete and Genome-Free Hepatitis B Virions Through Interfering With the Glycosylation of the HBV Envelope.Frontiers in microbiology · 2020Article
- SERINC5 Is an Unconventional HIV Restriction Factor That Is Upregulated during Myeloid Cell Differentiation.Journal of innate immunity · 2020Article
- Multifunctional Roles of the N-Terminal Region of HIV-1Journal of virology · 2019Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
It has recently emerged that HIV-1 Nef counteracts the antiviral host proteins SERINC3 and SERINC5. In particular, SERINC5 inhibits the infectivity of progeny virions when incorporated. SERINC3 and SERINC5 are also counteracted by the unrelated murine leukemia virus glycosylated Gag (glycoGag) protein, which possesses a potent Nef-like activity on HIV-1 infectivity. We now report that a minimal glycoGag termed glycoMA can fully substitute for Nef in promoting HIV-1 replication in Jurkat T lymphoid cells, indicating that Nef enhances replication in these cells mainly by counteracting SERINCs. In contrast, the SERINC antagonist glycoMA was unable to substitute for Nef in MOLT-3 T lymphoid cells, in which HIV-1 replication was highly dependent on Nef, and remained so even in the absence of SERINC3 and SERINC5. As in MOLT-3 cells, glycoMA was unable to substitute for Nef in stimulating HIV-1 replication in primary human cells. Although the ability of Nef mutants to promote HIV-1 replication in MOLT-3 cells correlated with the ability to engage endocytic machinery and to downregulate CD4, Nef nevertheless rescued virus replication under conditions where CD4 downregulation did not occur. Taken together, our observations raise the possibility that Nef triggers the endocytosis of a novel antiviral factor that is active against both laboratory-adapted and primary HIV-1 strains.
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Registered trials
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