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Clinical and Genotypic Findings in HIV-Infected Patients With the K65R Mutation Failing First-Line Antiretroviral Therapy in Nigeria

Hawkins, Claudia A MD, MPH, DTM&H*; Chaplin, Beth BA; Idoko, John MD; Ekong, Ernest MD, MPH§; Adewole, Isaac MD; Gashau, Wadzani MD; Murphy, Robert L MD*; Kanki, Phyllis D.V.M, SDand APIN Plus/Harvard PEPFAR Team

JAIDS Journal of Acquired Immune Deficiency Syndromes: October 2009 - Volume 52 - Issue 2 - p 228-234
doi: 10.1097/QAI.0b013e3181b06125
Clinical Science

Introduction: The HIV-1 epidemic in African countries is largely due to non-B HIV-1 subtypes. Patterns and frequency of antiretroviral drug resistance mutations observed in these countries may differ from those in the developed world, where HIV-1 subtype B predominates.

Methods: HIV-1 subtype and drug resistance mutations were assayed among Nigerian patients with treatment failure on first-line therapy (plasma HIV RNA >1000 copies/mL). Sequence analysis of the reverse transcriptase and protease gene revealed drug resistance mutations and HIV-1 viral subtype. Specific patterns of mutations and clinical characteristics are described in patients with the K65R mutation.

Results: Since 2005, 338 patients were evaluated. The most prevalent subtypes were CRF02_AG [152 of 338 (44.9%)] and G [128 of 338 (37.9%)]. Three hundred seven of 338 (90.8%) patients had previously received stavudine and/or zidovudine + lamivudine + efavirenz or nevirapine; 41 of 338 (12.1%) had received tenofovir (TDF). The most common nucleoside reverse transcriptase inhibitor mutations observed were M184V (301, 89.1%) and K70R (91, 26.9%). The K65R mutation was present in 37 of 338 patients (10.9%). The Q151M (P < 0.05), K219R, and T69del (P < 0.01) mutations were more common in patients with K65R who had not received TDF.

Conclusions: The K65R mutation is increasingly recognized and is a challenging finding among patients with non-B HIV subtypes, whether or not they have been exposed to TDF.

From the *Northwestern University, Chicago, IL; †Harvard School of Public Health, Boston, MA; ‡Jos University Teaching Hospital, Plateau State, Nigeria; §National Institute of Medical Research, Lagos, Nigeria; ‖University College Hospital, Ibadan, Nigeria; and ¶University of Maiduguri Teaching Hospital, Maiduguri, Nigeria.

Received for publication November 25, 2008; accepted May 11, 2009.

Supported by National Institutes for Health, #UO1 AI025915; AIDS Prevention Initiative in Nigeria, Bill & Melinda Gates Foundation; and Health Resources and Services Administration U51HA02522.

Presented in part as a poster presentation at the XVI International HIV Drug Resistance Workshop, June 12-16, 2007, Barbados, WI; and as a poster presentation at the 8th Antiviral Symposium on Antiviral Drug Resistance, November 11-14, 2007, Richmond, VA.

The contents are solely the responsibility of the authors and do not necessarily represent the official views of the funding institutions.

All authors have no Potential conflicts of interest.

GenBank accession numbers: FJ931123-FJ931460.

Correspondence to: Claudia Hawkins, MD, MPH, DTM&H, Division of Infectious Diseases, Northwestern University, 645 North Michigan, Suite 900, Chicago, IL 60611 (e-mail:

© 2009 Lippincott Williams & Wilkins, Inc.