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Journal of Virology, June 2008, p. 5653-5656, Vol. 82, No. 11
0022-538X/08/$08.00+0 doi:10.1128/JVI.00145-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Aaron Diamond AIDS Research Center, The Rockefeller University, 455 First Ave., 7th Floor, New York, New York 10016,1 Tulane National Primate Research Center, Tulane University Medical Center, 18702 Three Rivers Road, Covington, Louisiana 704332
Received 20 January 2008/ Accepted 25 March 2008
We report here a second case of coreceptor switch in R5 simian-human immunodeficiency virus SF162P3N (SHIVSF162P3N)-infected macaque CA28, supporting the use of this experimental system to examine factors that drive the change in coreceptor preference in vivo. Virus recovered from CA28 plasma (SHIVCA28NP) used both CCR5 and CXCR4 for entry, but the virus recovered from lymph node (SHIVCA28NL) used CXCR4 almost exclusively. Sequence and functional analyses showed that mutations in the V3 loop that conferred CXCR4 usage in macaque CA28 differed from those described in the previously reported case, demonstrating divergent mutational pathways for change in the coreceptor preference of the R5 SHIVSF162P3N isolate in vivo.
Published ahead of print on 2 April 2008.
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