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Journal of Virology, July 2003, p. 7682-7688, Vol. 77, No. 13
0022-538X/03/$08.00+0     DOI: 10.1128/JVI.77.13.7682-7688.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

High Frequency of Syncytium-Inducing and CXCR4-Tropic Viruses among Human Immunodeficiency Virus Type 1 Subtype C-Infected Patients Receiving Antiretroviral Treatment

Elizabeth R. Johnston,1* Lynn S. Zijenah,2 Solomon Mutetwa,3 Rami Kantor,1 Chonticha Kittinunvorakoon,4 and David A. Katzenstein1

Division of Infectious Diseases and AIDS Research, Stanford University, Stanford,1 Viral and Rickettsial Disease Laboratory, California Department of Health Services, Richmond, California,4 Immunology,2 Medical Microbiology, University of Zimbabwe Medical School, Harare, Zimbabwe3

Received 16 December 2002/ Accepted 4 April 2003

Human immunodeficiency virus type 1 (HIV-1) subtype C viruses have been found to almost exclusively use the chemokine receptor CCR5 as a coreceptor for entry, even in patients with advanced AIDS. We have characterized subtype C virus isolates from 28 patients from Harare, Zimbabwe, 20 of whom were receiving antiretroviral treatment. Virus from 10 of the treated patients induced syncytium formation (SI virus) when cultured with MT2 cells. Only non-syncytium-inducing (NSI) virus was cultured from the peripheral blood mononuclear cells of the eight patients who had not received treatment. The majority of these subtype C SI viruses were capable of using both CCR5 and CXCR4 as coreceptors for viral entry, and the consensus V3 loop sequences from the SI viruses displayed a high net charge compared to those of NSI viruses. While those on treatment had reverse transcriptase (RT) and protease mutations, there was no clear association between RT and protease drug resistance mutations and coreceptor tropism. These results suggest that CXCR4-tropic viruses are present within the quasispecies of patients infected with subtype C virus and that antiretroviral treatment may create an environment for the emergence of CXCR4 tropism.

* Corresponding author. Mailing address: Division of Infectious Diseases, Room S-156, Stanford University Medical Center, 300 Pasteur Dr., Stanford, CA 94035. Phone: (650) 498-5063. Fax: (650) 498-7011. E-mail: betsyj{at}stanford.edu.

Journal of Virology, July 2003, p. 7682-7688, Vol. 77, No. 13
0022-538X/03/$08.00+0     DOI: 10.1128/JVI.77.13.7682-7688.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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