HIV-1 vif mediates ubiquitination of the proximal protomer in the APOBEC3H dimer to induce degradation

Abstract The APOBEC3 family of cytidine deaminases restricts retroviruses like HIV-1 by mutating viral DNA. HIV-1 evades this restriction by producing Vif, which recruits the Cullin-5 (CUL5) E3 ubiquitin ligase complex to promote APOBEC3 degradation. Here we resolve key aspects of this counter-defen...

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Main Authors: Katarzyna A. Skorupka, Kazuhiro Matsuoka, Bakar Hassan, Rodolfo Ghirlando, Vanivilasini Balachandran, Ting-Hua Chen, Kylie J. Walters, Celia A. Schiffer, Matthias Wolf, Yasumasa Iwatani, Hiroshi Matsuo
Format: Article
Language:English
Published: Nature Portfolio 2025-07-01
Series:Nature Communications
Online Access:https://doi.org/10.1038/s41467-025-60984-y
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author Katarzyna A. Skorupka
Kazuhiro Matsuoka
Bakar Hassan
Rodolfo Ghirlando
Vanivilasini Balachandran
Ting-Hua Chen
Kylie J. Walters
Celia A. Schiffer
Matthias Wolf
Yasumasa Iwatani
Hiroshi Matsuo
author_facet Katarzyna A. Skorupka
Kazuhiro Matsuoka
Bakar Hassan
Rodolfo Ghirlando
Vanivilasini Balachandran
Ting-Hua Chen
Kylie J. Walters
Celia A. Schiffer
Matthias Wolf
Yasumasa Iwatani
Hiroshi Matsuo
author_sort Katarzyna A. Skorupka
collection DOAJ
description Abstract The APOBEC3 family of cytidine deaminases restricts retroviruses like HIV-1 by mutating viral DNA. HIV-1 evades this restriction by producing Vif, which recruits the Cullin-5 (CUL5) E3 ubiquitin ligase complex to promote APOBEC3 degradation. Here we resolve key aspects of this counter-defense mechanism by determining a 3.6 Å cryo-EM structure of chimpanzee APOBEC3H (cpzA3H) in complex with HIV-1 Vif and three components of the CUL5 E3 ligase-CBFβ, EloB, and EloC (VCBC). The structure captures cpzA3H as an RNA-mediated dimer within the cpzA3H-VCBC complex, allowing us to examine the role of dimerization. We find that ubiquitination occurs specifically at two lysine residues on the Vif-proximal protomer, while the distal protomer remains unmodified. The structural model of the active cpzA3H–Vif–CUL5 E3 ligase holoenzyme reveals spatial preferences for ubiquitin transfer to the targeted lysine residues. These findings enhance our understanding of A3H degradation and suggest new antiviral strategies targeting this host-virus interface.
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issn 2041-1723
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spelling doaj-art-115e91a1bde54facbd57e105a06fbfe82025-08-20T04:01:35ZengNature PortfolioNature Communications2041-17232025-07-0116111610.1038/s41467-025-60984-yHIV-1 vif mediates ubiquitination of the proximal protomer in the APOBEC3H dimer to induce degradationKatarzyna A. Skorupka0Kazuhiro Matsuoka1Bakar Hassan2Rodolfo Ghirlando3Vanivilasini Balachandran4Ting-Hua Chen5Kylie J. Walters6Celia A. Schiffer7Matthias Wolf8Yasumasa Iwatani9Hiroshi Matsuo10Cancer Innovation Laboratory, Frederick National Laboratory for Cancer ResearchClinical Research Center, National Hospital Organization Nagoya Medical CenterProtein Processing Section, Center for Structural Biology, Center for Cancer Research, National Cancer Institute, National Institutes of HealthLaboratory of Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, DHHSCancer Innovation Laboratory, Frederick National Laboratory for Cancer ResearchMolecular Cryo-Electron Microscopy Unit, Okinawa Institute of Science and Technology Graduate UniversityProtein Processing Section, Center for Structural Biology, Center for Cancer Research, National Cancer Institute, National Institutes of HealthDepartment of Biochemistry and Molecular Biotechnology, University of Massachusetts Chan Medical SchoolMolecular Cryo-Electron Microscopy Unit, Okinawa Institute of Science and Technology Graduate UniversityClinical Research Center, National Hospital Organization Nagoya Medical CenterCancer Innovation Laboratory, Frederick National Laboratory for Cancer ResearchAbstract The APOBEC3 family of cytidine deaminases restricts retroviruses like HIV-1 by mutating viral DNA. HIV-1 evades this restriction by producing Vif, which recruits the Cullin-5 (CUL5) E3 ubiquitin ligase complex to promote APOBEC3 degradation. Here we resolve key aspects of this counter-defense mechanism by determining a 3.6 Å cryo-EM structure of chimpanzee APOBEC3H (cpzA3H) in complex with HIV-1 Vif and three components of the CUL5 E3 ligase-CBFβ, EloB, and EloC (VCBC). The structure captures cpzA3H as an RNA-mediated dimer within the cpzA3H-VCBC complex, allowing us to examine the role of dimerization. We find that ubiquitination occurs specifically at two lysine residues on the Vif-proximal protomer, while the distal protomer remains unmodified. The structural model of the active cpzA3H–Vif–CUL5 E3 ligase holoenzyme reveals spatial preferences for ubiquitin transfer to the targeted lysine residues. These findings enhance our understanding of A3H degradation and suggest new antiviral strategies targeting this host-virus interface.https://doi.org/10.1038/s41467-025-60984-y
spellingShingle Katarzyna A. Skorupka
Kazuhiro Matsuoka
Bakar Hassan
Rodolfo Ghirlando
Vanivilasini Balachandran
Ting-Hua Chen
Kylie J. Walters
Celia A. Schiffer
Matthias Wolf
Yasumasa Iwatani
Hiroshi Matsuo
HIV-1 vif mediates ubiquitination of the proximal protomer in the APOBEC3H dimer to induce degradation
Nature Communications
title HIV-1 vif mediates ubiquitination of the proximal protomer in the APOBEC3H dimer to induce degradation
title_full HIV-1 vif mediates ubiquitination of the proximal protomer in the APOBEC3H dimer to induce degradation
title_fullStr HIV-1 vif mediates ubiquitination of the proximal protomer in the APOBEC3H dimer to induce degradation
title_full_unstemmed HIV-1 vif mediates ubiquitination of the proximal protomer in the APOBEC3H dimer to induce degradation
title_short HIV-1 vif mediates ubiquitination of the proximal protomer in the APOBEC3H dimer to induce degradation
title_sort hiv 1 vif mediates ubiquitination of the proximal protomer in the apobec3h dimer to induce degradation
url https://doi.org/10.1038/s41467-025-60984-y
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