This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow E-mail this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Google Scholar
Right arrow Articles by Yamashita, M.
Right arrow Articles by Emerman, M.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Yamashita, M.
Right arrow Articles by Emerman, M.

 Previous Article  |  Next Article 

Journal of Virology, October 2009, p. 9835-9843, Vol. 83, No. 19
0022-538X/09/$08.00+0     doi:10.1128/JVI.01084-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Cellular Restriction Targeting Viral Capsids Perturbs Human Immunodeficiency Virus Type 1 Infection of Nondividing Cells{triangledown}

Masahiro Yamashita and Michael Emerman*

Division of Human Biology, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109

Received 27 May 2009/ Accepted 13 July 2009

The ability of human immunodeficiency virus (HIV) to infect nondividing cells is a fundamental property by which HIV replicates in critical target cells, such as macrophages and resting CD4+ T cells. Recent studies have revealed that the capsid (CA) protein is a dominant factor that determines retrovirus infectivity in nondividing cells, and several mutations in HIV type 1 (HIV-1) CA abrogate the ability of HIV-1 to infect nondividing cells. We present evidence for a connection between cellular restriction against viral capsids and the resistance of nondividing cells to retrovirus infection. TRIM proteins that are able to target incoming viral capsids restrict HIV-1 more potently in nondividing cells than in dividing cells, thus rendering HIV-1 infection dependent on cell division. Moreover, cyclophilin A, another cellular protein that binds to HIV-1 CA, regulates HIV-1 infection of nondividing cells. Together, these data demonstrate the importance of capsid-binding cellular proteins in the control of the cell cycle independence of HIV-1. We propose that cellular restrictions to retroviral infections are themselves cell cycle dependent.

* Corresponding author. Mailing address: Division of Human Biology, Fred Hutchinson Cancer Research Center, 1100 Fairview Ave. N., P.O. Box 10924, Seattle, WA 98109. Phone: (206) 667-5058. Fax: (206) 667-6523. E-mail: memerman{at}fhcrc.org

{triangledown} Published ahead of print on 22 July 2009.

Journal of Virology, October 2009, p. 9835-9843, Vol. 83, No. 19
0022-538X/09/$08.00+0     doi:10.1128/JVI.01084-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





Copyright © 2010 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»