title: Characterization of drug resistance mutations in naïve and ART-treated patients infected with HIV-1 in Yaounde, Cameroon.
abstract: Currently the prevalence of HIV-1 infection in Cameroon is 5.1%, CRF02_AG subtype is responsible for about 50% of infections. Since an HIV-1 drug resistance test is not yet available widely, accurate data on the prevalence of resistant viral strains are missing. The objective of this study was to determine HIV-1 genetic diversity and to characterize HIV-1 mutations conferring drug resistance among antiretroviral therapy (ART)-naïve and ART-treated patients. A cohort of 239 patients infected with HIV were followed-up between January 2007 and July 2010 in Cameroon. Two hundred and sixteen plasma samples were sequenced for phylogenetic analysis and identification of drug resistance mutations in the HIV-1 pol region. A significant genetic diversity was found: Seven pure subtypes (A1, A3, D, F1, F2, G, H), nine circulating recombinant forms (CRFs: 01_AE, 02_AG, 06cpx, 09cpx, 11cpx, 13cpx, 16cpx, 18cpx, 37cpx) and one new unique recombinant form (URF) (G/F2). The rate of transmitted drug resistance (TDR) in naïve patients was 8.2% (4/49). Around 80% of patients failing a first-line ART harbored a virus with at least one resistance mutation to two antiretroviral (ARV) classes, and 36% of those failing a second-line regimen carried a virus with at least one resistant mutation to three ARV classes. The high level of drug resistance observed in the cohort is alarming because this occurred as a result of only few years of treatment. Adherence to therapy, adequate education of physicians, and the appropriate use of genotypic resistance assay are critical points of intervention for the improvement of patient care.
authors.affiliation: Clinical Infectious Disease, Tor Vergata University Hospital, Rome, Italy. ceccadoc@yahoo.it
authors.forename: Laura
authors.initials: L
authors.lastname: Ceccarelli
authors.forename: Romina
authors.initials: R
authors.lastname: Salpini
authors.forename: Sylvie
authors.initials: S
authors.lastname: Moudourou
authors.forename: Valeria
authors.initials: V
authors.lastname: Cento
authors.forename: Maria M
authors.initials: MM
authors.lastname: Santoro
authors.forename: Joseph
authors.initials: J
authors.lastname: Fokam
authors.forename: Desire
authors.initials: D
authors.lastname: Takou
authors.forename: Aubin
authors.initials: A
authors.lastname: Nanfack
authors.forename: Luca
authors.initials: L
authors.lastname: Dori
authors.forename: Judith
authors.initials: J
authors.lastname: Torimiro
authors.forename: Loredana
authors.initials: L
authors.lastname: Sarmati
authors.forename: Massimo
authors.initials: M
authors.lastname: Andreoni
authors.forename: Carlo F
authors.initials: CF
authors.lastname: Perno
authors.forename: Vittorio
authors.initials: V
authors.lastname: Colizzi
authors.forename: Giulia
authors.initials: G
authors.lastname: Cappelli
mesh_terms: D000328:Adult; D019380:Anti-HIV Agents / Q000494:pharmacology / Q000627:therapeutic use*; D002163:Cameroon / Q000453:epidemiology; D002648:Child; D002675:Child, Preschool; D003430:Cross-Sectional Studies; D024882:Drug Resistance, Viral / Q000235:genetics*; D005260:Female; D014644:Genetic Variation; D015658:HIV Infections / Q000188:drug therapy / Q000453:epidemiology* / Q000821:virology; D017320:HIV Protease Inhibitors / Q000494:pharmacology / Q000627:therapeutic use*; D015497:HIV-1 / Q000145:classification / Q000187:drug effects* / Q000235:genetics / Q000302:isolation & purification; D006801:Humans; D008297:Male; D009154:Mutation; D010802:Phylogeny; D015995:Prevalence; D011995:Recombination, Genetic; D018894:Reverse Transcriptase Inhibitors / Q000494:pharmacology / Q000627:therapeutic use*; D017422:Sequence Analysis, DNA; D017211:Treatment Failure; D054302:pol Gene Products, Human Immunodeficiency Virus / Q000235:genetics
chemical_list: D019380:Anti-HIV Agents; D017320:HIV Protease Inhibitors; D018894:Reverse Transcriptase Inhibitors; D054302:pol Gene Products, Human Immunodeficiency Virus