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Tetherin inhibits retrovirus release and is antagonized by HIV-1 Vpu

Author

Listed:
  • Stuart J. D. Neil

    (Aaron Diamond AIDS Research Center and Laboratory of Retrovirology, The Rockefeller University, 455 First Avenue, New York, New York 10016, USA)

  • Trinity Zang

    (Aaron Diamond AIDS Research Center and Laboratory of Retrovirology, The Rockefeller University, 455 First Avenue, New York, New York 10016, USA)

  • Paul D. Bieniasz

    (Aaron Diamond AIDS Research Center and Laboratory of Retrovirology, The Rockefeller University, 455 First Avenue, New York, New York 10016, USA)

Abstract

Human cells possess an antiviral activity that inhibits the release of retrovirus particles, and other enveloped virus particles, and is antagonized by the HIV-1 accessory protein, Vpu. This antiviral activity can be constitutively expressed or induced by interferon-α, and it consists of protein-based tethers, which we term ‘tetherins’, that cause retention of fully formed virions on infected cell surfaces. Using deductive constraints and gene expression analyses, we identify CD317 (also called BST2 or HM1.24), a membrane protein of previously unknown function, as a tetherin. Specifically, CD317 expression correlated with, and induced, a requirement for Vpu during HIV-1 and murine leukaemia virus particle release. Furthermore, in cells where HIV-1 virion release requires Vpu expression, depletion of CD317 abolished this requirement. CD317 caused retention of virions on cell surfaces and, after endocytosis, in CD317-positive compartments. Vpu co-localized with CD317 and inhibited these effects. Inhibition of Vpu function and consequent mobilization of tetherin’s antiviral activity is a potential therapeutic strategy in HIV/AIDS.

Suggested Citation

  • Stuart J. D. Neil & Trinity Zang & Paul D. Bieniasz, 2008. "Tetherin inhibits retrovirus release and is antagonized by HIV-1 Vpu," Nature, Nature, vol. 451(7177), pages 425-430, January.
    • Handle: RePEc:nat:nature:v:451:y:2008:i:7177:d:10.1038_nature06553
    DOI: 10.1038/nature06553
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    Cited by:

    1. Sylvie Rato & Antonio Rausell & Miguel Muñoz & Amalio Telenti & Angela Ciuffi, 2017. "Single-cell analysis identifies cellular markers of the HIV permissive cell," PLOS Pathogens, Public Library of Science, vol. 13(10), pages 1-23, October.
    2. Kerry L. Hilligan & Sivaranjani Namasivayam & Chad S. Clancy & Paul J. Baker & Samuel I. Old & Victoria Peluf & Eduardo P. Amaral & Sandra D. Oland & Danielle O’Mard & Julie Laux & Melanie Cohen & Nic, 2023. "Bacterial-induced or passively administered interferon gamma conditions the lung for early control of SARS-CoV-2," Nature Communications, Nature, vol. 14(1), pages 1-16, December.
    3. Nathaniel D Bachtel & Gisele Umviligihozo & Suzanne Pickering & Talia M Mota & Hua Liang & Gregory Q Del Prete & Pramita Chatterjee & Guinevere Q Lee & Rasmi Thomas & Mark A Brockman & Stuart Neil & M, 2018. "HLA-C downregulation by HIV-1 adapts to host HLA genotype," PLOS Pathogens, Public Library of Science, vol. 14(9), pages 1-25, September.
    4. Caterina Prelli Bozzo & Alexandre Laliberté & Aurora De Luna & Chiara Pastorio & Kerstin Regensburger & Stefan Krebs & Alexander Graf & Helmut Blum & Meta Volcic & Konstantin M. J. Sparrer & Frank Kir, 2024. "Replication competent HIV-guided CRISPR screen identifies antiviral factors including targets of the accessory protein Nef," Nature Communications, Nature, vol. 15(1), pages 1-17, December.
    5. Weijing Yang & Hong Wang & Zhaolong Li & Lihua Zhang & Jianhui Liu & Frank Kirchhoff & Chen Huan & Wenyan Zhang, 2024. "RPLP1 restricts HIV-1 transcription by disrupting C/EBPβ binding to the LTR," Nature Communications, Nature, vol. 15(1), pages 1-12, December.

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