Genetic determinants of HIV-1 subtype C Nef-mediated SERINC3 down-regulation

Abstract Background Nef-mediated down-regulation of the host restriction factors SERINC3 and SERINC5 significantly enhances HIV-1 infectivity. Natural Nef polymorphisms that affect SERINC3 down-regulation are not as well-characterised as those that affect SERINC5 down-regulation, particularly in HIV...

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Main Authors: Nikeisha Samlall, Tarylee Reddy, Nasreen Ismail, Mark A. Brockman, Zabrina L. Brumme, Thumbi Ndung’u, Jaclyn K. Mann
Format: Article
Language:English
Published: BMC 2025-04-01
Series:Virology Journal
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Online Access:https://doi.org/10.1186/s12985-025-02705-x
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author Nikeisha Samlall
Tarylee Reddy
Nasreen Ismail
Mark A. Brockman
Zabrina L. Brumme
Thumbi Ndung’u
Jaclyn K. Mann
author_facet Nikeisha Samlall
Tarylee Reddy
Nasreen Ismail
Mark A. Brockman
Zabrina L. Brumme
Thumbi Ndung’u
Jaclyn K. Mann
author_sort Nikeisha Samlall
collection DOAJ
description Abstract Background Nef-mediated down-regulation of the host restriction factors SERINC3 and SERINC5 significantly enhances HIV-1 infectivity. Natural Nef polymorphisms that affect SERINC3 down-regulation are not as well-characterised as those that affect SERINC5 down-regulation, particularly in HIV-1 subtype C infection. We therefore aimed to identify genetic determinants of SERINC3 down-regulation by subtype C Nef. In addition, we investigated the role of SERINC3 down-regulation activity in disease progression and its contribution to overall Nef function, using Nef fitness model-derived E values as a proxy for overall Nef function in vivo. Methods SERINC3 down-regulation activity of 107 participant-derived Nef clones was measured using a flow cytometry-based assay in a T cell line. The relationship between SERINC3 down-regulation activity and viral load set point or rate of CD4 + T cell decline during untreated HIV infection was analysed by linear regression. Quantile regression was used to assess the contribution of SERINC3 down-regulation activity to overall Nef function. Individual Nef amino acids associated with a significantly altered SERINC3 down-regulation activity were identified using codon-by-codon Mann Whitney U tests. Results SERINC3 down-regulation activity was not a significant predictor of viral load set point nor rate of CD4 + T cell decline. SERINC3 down-regulation activity was a significant predictor of estimated Nef fitness (E values) in univariate analysis (p < 0.0001) and remained significant in multivariate analyses adjusting for other Nef functions that were measured for the same Nef clones (p < 0.02). A total of 30 amino acids were identified to be associated with differential Nef-mediated ability to down-regulate SERINC3 (p < 0.05 and q < 0.3), with 63% of these residues being in the N-terminal domain. Conclusion Although SERINC3 down-regulation did not associate significantly with markers of HIV disease progression, our results nevertheless suggest that SERINC3 down-regulation contributes significantly to overall Nef function and fitness. The identification of Nef amino acids associated with differential SERINC3 down-regulation ability may be useful for rational design of therapeutics and vaccines targeting the Nef region.
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spelling doaj-art-d70fe6f8051e4351b0717a7904d5960d2025-08-20T02:17:04ZengBMCVirology Journal1743-422X2025-04-0122111110.1186/s12985-025-02705-xGenetic determinants of HIV-1 subtype C Nef-mediated SERINC3 down-regulationNikeisha Samlall0Tarylee Reddy1Nasreen Ismail2Mark A. Brockman3Zabrina L. Brumme4Thumbi Ndung’u5Jaclyn K. Mann6HIV Pathogenesis Programme, The Doris Duke Medical Research Institute, University of Kwazulu-NatalMedical Research Council, Biostatistics UnitHIV Pathogenesis Programme, The Doris Duke Medical Research Institute, University of Kwazulu-NatalFaculty of Health Sciences, Simon Fraser UniversityFaculty of Health Sciences, Simon Fraser UniversityHIV Pathogenesis Programme, The Doris Duke Medical Research Institute, University of Kwazulu-NatalHIV Pathogenesis Programme, The Doris Duke Medical Research Institute, University of Kwazulu-NatalAbstract Background Nef-mediated down-regulation of the host restriction factors SERINC3 and SERINC5 significantly enhances HIV-1 infectivity. Natural Nef polymorphisms that affect SERINC3 down-regulation are not as well-characterised as those that affect SERINC5 down-regulation, particularly in HIV-1 subtype C infection. We therefore aimed to identify genetic determinants of SERINC3 down-regulation by subtype C Nef. In addition, we investigated the role of SERINC3 down-regulation activity in disease progression and its contribution to overall Nef function, using Nef fitness model-derived E values as a proxy for overall Nef function in vivo. Methods SERINC3 down-regulation activity of 107 participant-derived Nef clones was measured using a flow cytometry-based assay in a T cell line. The relationship between SERINC3 down-regulation activity and viral load set point or rate of CD4 + T cell decline during untreated HIV infection was analysed by linear regression. Quantile regression was used to assess the contribution of SERINC3 down-regulation activity to overall Nef function. Individual Nef amino acids associated with a significantly altered SERINC3 down-regulation activity were identified using codon-by-codon Mann Whitney U tests. Results SERINC3 down-regulation activity was not a significant predictor of viral load set point nor rate of CD4 + T cell decline. SERINC3 down-regulation activity was a significant predictor of estimated Nef fitness (E values) in univariate analysis (p < 0.0001) and remained significant in multivariate analyses adjusting for other Nef functions that were measured for the same Nef clones (p < 0.02). A total of 30 amino acids were identified to be associated with differential Nef-mediated ability to down-regulate SERINC3 (p < 0.05 and q < 0.3), with 63% of these residues being in the N-terminal domain. Conclusion Although SERINC3 down-regulation did not associate significantly with markers of HIV disease progression, our results nevertheless suggest that SERINC3 down-regulation contributes significantly to overall Nef function and fitness. The identification of Nef amino acids associated with differential SERINC3 down-regulation ability may be useful for rational design of therapeutics and vaccines targeting the Nef region.https://doi.org/10.1186/s12985-025-02705-xHIV-1NefHIV-1 subtype CSERINC3 down-regulationSERINC5 down-regulation
spellingShingle Nikeisha Samlall
Tarylee Reddy
Nasreen Ismail
Mark A. Brockman
Zabrina L. Brumme
Thumbi Ndung’u
Jaclyn K. Mann
Genetic determinants of HIV-1 subtype C Nef-mediated SERINC3 down-regulation
Virology Journal
HIV-1
Nef
HIV-1 subtype C
SERINC3 down-regulation
SERINC5 down-regulation
title Genetic determinants of HIV-1 subtype C Nef-mediated SERINC3 down-regulation
title_full Genetic determinants of HIV-1 subtype C Nef-mediated SERINC3 down-regulation
title_fullStr Genetic determinants of HIV-1 subtype C Nef-mediated SERINC3 down-regulation
title_full_unstemmed Genetic determinants of HIV-1 subtype C Nef-mediated SERINC3 down-regulation
title_short Genetic determinants of HIV-1 subtype C Nef-mediated SERINC3 down-regulation
title_sort genetic determinants of hiv 1 subtype c nef mediated serinc3 down regulation
topic HIV-1
Nef
HIV-1 subtype C
SERINC3 down-regulation
SERINC5 down-regulation
url https://doi.org/10.1186/s12985-025-02705-x
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