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J Virol, March 1998, p. 2491-2495, Vol. 72, No. 3
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Coreceptor Utilization by Human Immunodeficiency Virus Type 1 Is Not a Primary Determinant of Neutralization Sensitivity

Rachel A. Lacasse,1 Kathryn E. Follis,1 Tarsem Moudgil,1 Meg Trahey,1 James M. Binley,2 Vicente Planelles,3 Susan Zolla-Pazner,4,5 and Jack H. Nunberg1,*

Montana Biotechnology Center, The University of Montana, Missoula, Montana 598121; Aaron Diamond AIDS Research Center and The Rockefeller University, New York, New York 100162; University of Rochester Cancer Center, Rochester, New York 146423; and Veterans Affairs4 and New York University5 Medical Centers, New York, New York 10010

Received 24 September 1997/Accepted 4 December 1997

We have examined the relationship between coreceptor utilization and sensitivity to neutralization in a primary isolate of human immunodeficiency virus type 1 and its T-cell line-adapted (TCLA) derivative. We determined that adaptation of the primary-isolate (PI) virus 168P results in the loss of the unique capacity of PI viruses to utilize the CCR5 coreceptor and in the acquisition by the TCLA 168C virus of sensitivity to neutralization by V3-directed monoclonal antibodies (MAbs). In experiments wherein infection by 168P is directed via either the CCR5 or the CXCR4 pathway, we demonstrate that the virus, as well as pseudotyped virions bearing a molecularly cloned 168P envelope protein, remains refractory to neutralization by MAbs 257-D, 268-D, and 50.1 regardless of the coreceptor utilized. This study suggests that coreceptor utilization is not a primary determinant of differential neutralization sensitivity in PI and TCLA viruses.

* Corresponding author. Mailing address: Montana Biotechnology Center, The University of Montana, Missoula, MT 59812. Phone: (406) 243-6421. Fax: (406) 243-6425. E-mail: nunberg{at}selway.umt.edu.




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Copyright © 1998 by the American Society for Microbiology. All rights reserved.