ArticleScientific reports2020
Impaired ability of Nef to counteract SERINC5 is associated with reduced plasma viremia in HIV-infected individuals.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The trial behind it
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- HIV-1 Nef Uses a Conserved Pocket to Recruit the N-Terminal Cytoplasmic Tail of Serinc3.Viruses · 2025Article
- Genetic determinants of HIV-1 subtype C Nef-mediated SERINC3 down-regulation.Virology journal · 2025Article
- Beyond Impairment of Virion Infectivity: New Activities of the Anti-HIV Host Cell Factor SERINC5.Viruses · 2024Review
- SERINC5 counters retroviruses and non-retroviruses.Frontiers in cellular and infection microbiology · 2024Review
- HIV-1 restriction by SERINC5.Medical microbiology and immunology · 2023Review
- HIV-1 subtype C Nef-mediated SERINC5 down-regulation significantly contributes to overall Nef activity.Retrovirology · 2023Article
- SERINC5 restricts influenza virus infectivity.PLoS pathogens · 2022Article
- The Emerging Role of the Serine Incorporator Protein Family in Regulating Viral Infection.Frontiers in cell and developmental biology · 2022Review
- Aromatic Side Chain at Position 412 of SERINC5 Exerts Restriction Activity toward HIV-1 and Other Retroviruses.Journal of virology · 2021Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
HIV-1 Nef plays an essential role in enhancing virion infectivity by antagonizing the host restriction molecule SERINC5. Because Nef is highly polymorphic due to the selective forces of host cellular immunity, we hypothesized that certain immune-escape polymorphisms may impair Nef's ability to antagonize SERINC5 and thereby influence viral fitness in vivo. To test this hypothesis, we identified 58 Nef polymorphisms that were overrepresented in HIV-infected patients in Japan sharing the same HLA genotypes. The number of immune-associated Nef polymorphisms was inversely correlated with the plasma viral load. By breaking down the specific HLA allele-associated mutations, we found that a number of the HLA-B*51:01-associated Y120F and Q125H mutations were most significantly associated with a reduced plasma viral load. A series of biochemical experiments showed that the double mutations Y120F/Q125H, but not either single mutation, impaired Nef's ability to antagonize SERINC5 and was associated with decreasing virion infectivity and viral replication in primary lymphocytes. In contrast, other Nef functions such as CD4, CCR5, CXCR4 and HLA class I downregulation and CD74 upregulation remained unchanged. Taken together, our results suggest that the differential ability of Nef to counteract SERINC5 by naturally occurring immune-associated mutations was associated with the plasma viral load in vivo.
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Registered trials
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