title: Analysis of the diversity of the HIV-1 pol gene and drug resistance associated changes among drug-naïve patients in Burkina Faso.
abstract: A cross-sectional study was undertaken among drug-naïve HIV patients at the University Hospital in Ouagadougou shortly before and after the introduction of large-scale antiretroviral therapy (ART) in Burkina Faso. Baseline clinical and virological data as well as protease (PR) and 5' reverse transcriptase (RT) sequences from 104 HIV infected patients were analyzed. Genotypic classification revealed the following subtypes and recombinant forms: CRF06_cpx, n = 46 (44.2%); CRF02_AG, n = 39 (37.5%); subtype A, n = 4 (3.8%); CRF09_cpx, n = 2 (1.9%); and unclassified, n = 13 (12.5%). Bootstrap analysis of CRF02_AG and CRF06_cpx viruses showed that >80% had a similar structure to their respective prototypes. The prevalence of primary drug resistance mutations was 12.5%, all mutations arising in the RT sequences in accordance with the dominance of this drug class in Burkina Faso. The mutations were distributed as follows: NRTI (10.6%): M41L (n = 2), D67N (n = 2), K70K/E (n = 2), L210W (n = 1), T215S/Y (n = 2), and K219K/Q (n = 2); NNRTI (6.1%): K103K/N (n = 2), Y181C (n = 2), G190G/A (n = 1), and P236P/L (n = 1). Subtype specific secondary polymorphisms such as K20I and M36I in the PR were observed in almost all patients. Drug resistance mutations occurred at similar frequencies (12.8% and 10.8%, respectively) among patients infected with CRF02_AG and CRF06_cpx. Some subtype specific polymorphisms were observed within important HLA epitopes, including B35, B7, and A2 in the RT, and A*6802 in the PR sequences. The observed resistance mutations are most likely to have been transmitted based on the timing of the study but prior undocumented use of ART cannot be excluded.
authors.affiliation: Abteilung Virologie, Universitaetsklinikum Heidelberg, Heidelberg, Germany.
authors.forename: Denis M
authors.initials: DM
authors.lastname: Tebit
authors.forename: Lassana
authors.initials: L
authors.lastname: Sangaré
authors.forename: Fabrice
authors.initials: F
authors.lastname: Tiba
authors.forename: Yameogo
authors.initials: Y
authors.lastname: Saydou
authors.forename: Aline
authors.initials: A
authors.lastname: Makamtse
authors.forename: Hermann
authors.initials: H
authors.lastname: Somlare
authors.forename: Guillaume
authors.initials: G
authors.lastname: Bado
authors.forename: Boris G
authors.initials: BG
authors.lastname: Kouldiaty
authors.forename: Inoussa
authors.initials: I
authors.lastname: Zabsonre
authors.forename: Sibiri L
authors.initials: SL
authors.lastname: Yameogo
authors.forename: Kanokporn
authors.initials: K
authors.lastname: Sathiandee
authors.forename: Joseph Y
authors.initials: JY
authors.lastname: Drabo
authors.forename: Hans-Georg
authors.initials: HG
authors.lastname: Kräusslich
mesh_terms: D000293:Adolescent; D000328:Adult; D002050:Burkina Faso; D002648:Child; D016000:Cluster Analysis; D003430:Cross-Sectional Studies; D024882:Drug Resistance, Viral; D005260:Female; D005838:Genotype; D015658:HIV Infections / Q000821:virology*; D016333:HIV Protease / Q000235:genetics; D054303:HIV Reverse Transcriptase / Q000235:genetics; D015497:HIV-1 / Q000187:drug effects* / Q000235:genetics* / Q000302:isolation & purification; D006801:Humans; D008297:Male; D008875:Middle Aged; D008969:Molecular Sequence Data; D020125:Mutation, Missense; D010802:Phylogeny; D011995:Recombination, Genetic; D017422:Sequence Analysis, DNA; D017385:Sequence Homology; D055815:Young Adult; D054302:pol Gene Products, Human Immunodeficiency Virus / Q000235:genetics*
chemical_list: D054302:pol Gene Products, Human Immunodeficiency Virus; C514824:reverse transcriptase, Human immunodeficiency virus 1; D054303:HIV Reverse Transcriptase; D016333:HIV Protease; C514803:p16 protease, Human immunodeficiency virus 1