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Journal of Virology, February 2003, p. 2587-2599, Vol. 77, No. 4
0022-538X/03/$08.00+0     DOI: 10.1128/JVI.77.4.2587-2599.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Molecular Characteristics of Human Immunodeficiency Virus Type 1 Subtype C Viruses from KwaZulu-Natal, South Africa: Implications for Vaccine and Antiretroviral Control Strategies

M. Gordon,1 T. De Oliveira,1 K. Bishop,1 H. M. Coovadia,2 L. Madurai,3 S. Engelbrecht,4 E. Janse van Rensburg,4 A. Mosam,5 A. Smith,6 and S. Cassol1,7*

HIV-1 Molecular Virology and Bioinformatics Laboratories, Africa Centre for Health and Population Studies and the Nelson R. Mandela School of Medicine,1 Centre for HIV/AIDS Networking,2 Department of Dermatology,5 Department of Virology, University of Natal,6 Medical Research Council, Durban,3 Department of Medical Virology, University of Stellenbosch and Tygerberg Hospital, Tygerberg, South Africa,4 Nuffield Department of Clinical Medicine, University of Oxford, Oxford, United Kingdom7

Received 29 July 2002/ Accepted 7 November 2002

The KwaZulu-Natal region of South Africa is experiencing an explosive outbreak of human immunodeficiency virus type 1 (HIV-1) subtype C infections. Understanding the genetic diversity of C viruses and the biological consequences of this diversity is important for the design of effective control strategies. We analyzed the protease gene, the first 935 nucleotides of reverse transcriptase, and the C2V5 envelope region of a representative set of 72 treatment-naïve patients from KwaZulu-Natal and correlated the results with amino acid signature and resistance patterns. Phylogenetic analysis revealed multiple clusters or "lineages" of HIV-1 subtype C that segregated with other C viruses from southern Africa. The same pattern was observed for both black and Indian subgroups and for retrospective specimens collected prior to 1990, indicating that multiple sublineages of HIV-1 C have been present in KwaZulu-Natal since the early stages of the epidemic. With the exception of three nonnucleoside reverse transcriptase inhibitor mutations, no primary resistance mutations were identified. Numerous accessory polymorphisms were present in the protease, but none were located at drug-binding or active sites of the enzyme. One frequent polymorphism, I93L, was located near the protease/reverse transcriptase cleavage site. In the envelope, disruption of the glycosylation motif at the beginning of V3 was associated with the presence of an extra protein kinase C phosphorylation site at codon 11. Many polymorphisms were embedded within cytotoxic T lymphocyte or overlapping cytotoxic T-lymphocyte/T-helper epitopes, as defined for subtype B. This work forms a baseline for future studies aimed at understanding the impact of genetic diversity on vaccine efficacy and on natural susceptibility to antiretroviral drugs.

* Corresponding author. Mailing address: HIV-1 Molecular Virology and Bioinformatics Laboratories, Africa Centre for Health and Population Studies, Nelson R. Mandela School of Medicine, University of Natal, Congella 4013, Durban, South Africa. Phone: 27 31 260 4013. Fax: 27 31 260 4015. E-mail: sharon.cassol{at}mrc.ac.za.

Journal of Virology, February 2003, p. 2587-2599, Vol. 77, No. 4
0022-538X/03/$08.00+0     DOI: 10.1128/JVI.77.4.2587-2599.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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