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Journal of Clinical Microbiology, November 2000, p. 3919-3925, Vol. 38, No. 11
0095-1137/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Genetic Diversity of Protease and Reverse Transcriptase Sequences in Non-Subtype-B Human Immunodeficiency Virus Type 1 Strains: Evidence of Many Minor Drug Resistance Mutations in Treatment-Naive Patients

Laurence Vergne,1 Martine Peeters,1,* Eitel Mpoudi-Ngole,2 Anke Bourgeois,2 Florian Liegeois,1 Coumba Toure-Kane,3 Souleymane Mboup,3 Claire Mulanga-Kabeya,1 Eric Saman,4 Jacques Jourdan,5 Jacques Reynes,6 and Eric Delaporte1,6

Laboratoire Retrovirus, IRD, Montpellier,1 CHU, Caremeau, 30029 Nimes cedex 4,5 and CHU, Gui de Chauliac, 34295 Montpellier Cedex 5,6 France; Projet PRESICA, BP 906, Yaounde, Cameroon2; CHU, Le Dantec, BP 7325, Dakar, Senegal3; and Innogenetics, 9052 Zwijnaarde, Belgium4

Received 24 February 2000/Returned for modification 11 May 2000/Accepted 17 July 2000

Most human immunodeficiency virus (HIV) drug susceptibility studies have involved subtype B strains. Little information on the impact of viral diversity on natural susceptibility to antiretroviral drugs has been reported. However, the prevalence of non-subtype-B (non-B) HIV type 1 (HIV-1) strains continues to increase in industrialized countries, and antiretroviral treatments have recently become available in certain developing countries where non-B subtypes predominate. We sequenced the protease and reverse transcriptase (RT) genes of 142 HIV-1 isolates from antiretroviral-naive patients: 4 belonged to group O and 138 belonged to group M (9 subtype A, 13 subtype B, 2 subtype C, 5 subtype D, 2 subtype F1, 9 subtype F2, 4 subtype G, 5 subtype J, 2 subtype K, 3 subtype CRF01-AE, 67 subtype CRF02-AG, and 17 unclassified isolates). No major mutations associated with resistance to nucleoside reverse transcriptase inhibitors (NRTIs) or protease inhibitors were detected. Major mutations linked to resistance to non-NRTI agents were detected in all group O isolates (A98G and Y181C) and in one subtype J virus (V108I). In contrast, many accessory mutations were found, especially in the protease gene. Only 5.6% of the 142 strains, all belonging to subtype B or D, had no mutations in the protease gene. Sixty percent had one mutation, 22.5% had two mutations, 9.8% had three mutations, and 2.1% (all group O strains) had four mutations. In order of decreasing frequency, the following mutations were identified in the protease gene: M36I (86.6%), L10I/V (26%), L63P (12.6%), K20M/R (11.2%), V77I (5.6%), A71V (2.8%), L33F (0.7%), and M46I (0.7%). R211K, an accessory mutation associated with NRTI resistance, was also observed in 43.6% of the samples. Phenotypic and clinical studies are now required to determine whether multidrug-resistant viruses emerge more rapidly during antiretroviral therapy when minor resistance-conferring mutations are present before treatment initiation.

* Corresponding author. Mailing address: Laboratoire Retrovirus, IRD, 911 Avenue Agropolis, BP 5045, 34032 Montpellier Cedex 1, France. Phone: 33-4 67 41 62 97. Fax: 33-4 67 61 94 50. E-mail: martine.peeters{at}mpl.ird.fr.

Journal of Clinical Microbiology, November 2000, p. 3919-3925, Vol. 38, No. 11
0095-1137/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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