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Journal of Virology, April 2007, p. 3657-3661, Vol. 81, No. 7
0022-538X/07/$08.00+0 doi:10.1128/JVI.02310-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.
Evolution of CXCR4-Using Human Immunodeficiency Virus Type 1 SF162 Is Associated with Two Unique Envelope Mutations
Yana Kiselyeva,1
Rebecca Nedellec,2
Alejandra Ramos,2
Cristina Pastore,2
Leonid B. Margolis,1* and
Donald E. Mosier2*
Laboratory of Molecular and Cellular Biophysics, National Institute of Child Health and Human Development, Bethesda, Maryland 20892,1
Department of Immunology, The Scripps Research Institute, La Jolla, California 920372
Received 20 October 2006/
Accepted 19 December 2006
CCR5-using human immunodeficiency virus type 1 (HIV-1) isolates typically gain CXCR4 use via multiple mutations in V3 and often V1/V2 regions of envelope, and patterns of mutations are distinct for each isolate. Here, we report that multiple CXCR4-using variants of a parental CCR5-using HIV-1 isolate, SF162, obtained by either target cell selection or CCR5 inhibition have a common mutation pattern characterized by the same two V3 mutations and that these mutations preexisted in some of the SF162 stocks. These results imply that SF162 has a single pathway for acquiring CXCR4 use and that prolonged culture is sufficient to select for R5X4 variants.
* Corresponding author. Mailing address for Leonid B. Margolis: Laboratory of Molecular and Cellular Biophysics, NICHD, NIH, 10 Center Drive, 10/9D58, Bethesda, MD 20892. Phone: (301) 594-2476. Fax: (301) 480-0850. E-mail:
margolis{at}helix.nih.gov. Mailing address for Donald E. Mosier: Department of Immunology-IMM7, The Scripps Research Institute, 10550 N. Torrey Pines Road, La Jolla, CA 92037. Phone: (858) 784-9121. Fax: (858) 784-9190. E-mail:
dmosier{at}scripps.edu.
Published ahead of print on 3 January 2007.
Journal of Virology, April 2007, p. 3657-3661, Vol. 81, No. 7
0022-538X/07/$08.00+0 doi:10.1128/JVI.02310-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.
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