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Beyond Tsg101: the role of Alix in 'ESCRTing' HIV-1

Nature Reviews Microbiology volume 5, pages 912916 (2007) | Download Citation

Abstract

The limited coding capacity of retroviral genomes forces these viruses to rely heavily on the host-cell machinery for their replication. This phenomenon is particularly well illustrated by the interaction between retroviruses and components of the endosomal budding machinery that occurs during virus release. Here, we focus on the use of host-cell factors during HIV-1 budding and highlight recent progress in our understanding of the role of one such factor, Alix, in both viral and cellular membrane budding and fission events.

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Acknowledgements

The authors thank W. S. Hu, V. Pathak and members of the Freed laboratory for the critical review of the manuscript. Work in the authors' laboratories is supported by intramural grant support from the Center for Cancer Research, the National Cancer Institute, the National Institute of Diabetes and Digestive and Kidney Diseases and the Intramural AIDS Targeted Antiviral Program.

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Affiliations

  1. Ken Fujii and Eric O. Freed are at the Virus–Cell Interaction Section, HIV Drug Resistance Program, National Cancer Institute, Frederick, Maryland 21702-1201, USA.

    • Ken Fujii
    •  & Eric O. Freed
  2. James H. Hurley is at the Laboratory of Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA.

    • James H. Hurley

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Correspondence to Eric O. Freed.

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DOI

https://doi.org/10.1038/nrmicro1790

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