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Journal of Clinical Microbiology, March 2002, p. 837-845, Vol. 40, No. 3
0095-1137/02/$04.00+0     DOI: 10.1128/JCM.40.3.837-845.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Human Immunodeficiency Virus Type 1 Group M Protease in Cameroon: Genetic Diversity and Protease Inhibitor Mutational Features

Peter N. Fonjungo,¹ Eitel N. Mpoudi,² Judith N. Torimiro,² George A. Alemnji,² Laura T. Eno,² Esther J. Lyonga,² John N. Nkengasong,^3,4 Renu B. Lal,⁵ Mark Rayfield,¹ Marcia L. Kalish,¹ Thomas M. Folks,¹ and Danuta Pieniazek^1*

HIV and Retrovirology Branch,¹ HIV Immunology and Diagnostics Branch, Division of AIDS, STD, and TB Laboratory Research, National Center for Infectious Diseases,⁵ Division of HIV/AIDS Prevention, National Center for HIV, STD, and TB Prevention, Centers for Disease ControlPrevention, Atlanta, Georgia,⁴ Hôpital Militaire de Yaoundé, Yaoundé, Cameroon,² Projet RETRO-CI, Abidjan, Côte d'Ivoire³

Received 21 August 2001/ Returned for modification 4 October 2001/ Accepted 14 December 2001

To establish a baseline for monitoring resistance to protease inhibitors (PIs) and examining the efficacy of their use among persons in Cameroon infected with human immunodeficiency virus type 1 (HIV-1), we analyzed genetic variability and PI resistance-associated substitutions in PCR-amplified protease (PR) sequences in strains isolated from 110 HIV-1-infected, drug-naïve Cameroonians. Of the 110 strains, 85 were classified into six HIV-1 PR subtypes, A (n = 1), B (n = 1), F (n = 4), G (n = 7), H (n = 1), and J (n = 7), and a circulating recombinant form, CRF02-AG (n = 64). PR genes from the remaining 25 (23%) specimens were unclassifiable, whereas 2% (7 of 301) unclassifiable PR sequences were reported for a global collection. Two major PI resistance-associated mutations, 20M and 24I, were detected in strains from only two specimens, whereas secondary mutations were found in strains from all samples except one strain of subtype B and two strains of CRF02-AG. The secondary mutations showed the typical PI resistance-associated pattern for non-subtype B viruses in both classifiable and unclassifiable PR genes, with 36I being the predominant (99%) mutation, followed by 63P (18%), 20R (15%), 77I (13%), and 10I or 10V (11%). Of these mutations, dual and triple PI resistance-associated substitutions were found in 38% of all the Cameroonian strains. Compared with classifiable PR sequences, unclassifiable sequences had significantly more dual and triple substitutions (64% versus 30%; P = 0.004). Phenotypic and clinical evaluations are needed to estimate whether PI resistance during antiretroviral drug treatment occurs more rapidly in individuals infected with HIV-1 strains harboring multiple PI resistance-associated substitutions. This information may be important for determination of appropriate drug therapies for HIV-1-infected persons in Cameroon, where more than one-third of HIV-1 strains were found to carry dual and triple minor PI resistance-associated mutations.

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* Corresponding author. Mailing address: HIV and Retrovirology Branch, CDC, 1600 Clifton Rd., Mailstop G-19, Atlanta, GA 30333. Phone: (404) 639-1008. Fax: (404) 639-1174. E-mail: dxp1{at}cdc.gov.

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Journal of Clinical Microbiology, March 2002, p. 837-845, Vol. 40, No. 3
0095-1137/02/$04.00+0     DOI: 10.1128/JCM.40.3.837-845.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

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