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
Services
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
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Kim, J.-O.
Right arrow Articles by Nabel, G. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kim, J.-O.
Right arrow Articles by Nabel, G. J.

 Previous Article  |  Next Article 

Journal of Virology, February 2007, p. 1444-1450, Vol. 81, No. 3
0022-538X/07/$08.00+0     doi:10.1128/JVI.01790-06

Lysis of Human Immunodeficiency Virus Type 1 by a Specific Secreted Human Phospholipase A2{triangledown}

Jae-Ouk Kim, Bimal K. Chakrabarti, Anuradha Guha-Niyogi, Mark K. Louder, John R. Mascola, Lakshmanan Ganesh,{dagger} and Gary J. Nabel*

Vaccine Research Center, NIAID, National Institutes of Health, Room 4502, Bldg. 40, MSC-3005, 40 Convent Drive, Bethesda, Maryland 20892-3005

Received 17 August 2006/ Accepted 31 October 2006

Phospholipase A2 (PLA2) proteins affect cellular activation, signal transduction, and possibly innate immunity. A specific secretory PLA2, sPLA2-X, is shown here to neutralize human immunodeficiency virus type 1 (HIV-1) through degradation of the viral membrane. Catalytic function was required for antiviral activity, and the target cells of infection were unaffected. sPLA2-X potently reduced gene transfer of HIV-1 Env-pseudotyped lentivirus vectors and inhibited the replication of both CCR5- and CXCR4-tropic HIV-1 in human CD4+ T cells. Virions resistant to damage by antibody and complement were sensitive to lysis by sPLA2-X, suggesting a novel mechanism of antiviral surveillance independent of the acquired immune system.

* Corresponding author. Mailing address: Vaccine Research Center, NIAID, National Institutes of Health, Room 4502, Bldg. 40, MSC-3005, 40 Convent Dr., Bethesda, MD 20892-3005. Phone: (301) 496-1852. Fax: (301) 480-0274. E-mail: gnabel{at}nih.gov.

{triangledown} Published ahead of print on 8 November 2006.

{dagger} Deceased.

Journal of Virology, February 2007, p. 1444-1450, Vol. 81, No. 3
0022-538X/07/$08.00+0     doi:10.1128/JVI.01790-06




This article has been cited by other articles:

  • Pindado, J., Balsinde, J., Balboa, M. A. (2007). TLR3-Dependent Induction of Nitric Oxide Synthase in RAW 264.7 Macrophage-Like Cells via a Cytosolic Phospholipase A2/Cyclooxygenase-2 Pathway. J. Immunol. 179: 4821-4828 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»