title: High prevalence of unique recombinant forms of HIV-1 in Ghana: molecular epidemiology from an antiretroviral resistance study.
abstract: BACKGROUND
  In Ghana, programs to expand antiretroviral access are being implemented. In this context, the dynamic genetic evolution of HIV-1 requires continuous surveillance, particularly when diverse genetic forms co-circulate.
  
  
  METHODS
  Phylogenetic and antiretroviral resistance analyses of HIV-1 partial pol sequences from plasma RNA samples from 207 Ghanaian individuals were performed.
  
  
  RESULTS
  66% of infections were CRF02_AG, whereas 25% were unique recombinant forms (URFs). All 52 URFs were characterized by bootscanning. CRF02_AG was parental strain in 87% of URFs, forming recombinants with genetic forms circulating in minor proportions: CRF06_cpx, sub-subtype A3, CRF09_cpx and subtypes G and D. Two triple recombinants (CRF02_AG/A3/CRF06_cpx and CRF02_AG/A3/CRF09_cpx) were identified. Antiretroviral resistance analyses revealed that six individuals, five of which were antiretroviral drug-experienced, harbored mutations conferring high level of resistance to reverse transcriptase inhibitors. No major resistance mutations were identified in the protease, although insertions of one and three amino acids were detected.
  
  
  CONCLUSIONS
  The high frequency of URFs detected probably reflects a significant incidence of coinfections or superinfections with diverse viral strains, which increases the genetic complexity of the HIV-1 epidemic in West Africa. Monitoring of HIV-1 drug resistance might provide data on the implications of intersubtype recombination in response to antiretrovirals.
authors.affiliation: Viral Pathogenesis Department, Centro Nacional de Microbiología, Instituto de Salud Carlos III, Majadahonda, Madrid, Spain. delgade@isciii.es
authors.forename: Elena
authors.initials: E
authors.lastname: Delgado
authors.forename: William Kwabena
authors.initials: WK
authors.lastname: Ampofo
authors.forename: María
authors.initials: M
authors.lastname: Sierra
authors.forename: Kwasi
authors.initials: K
authors.lastname: Torpey
authors.forename: Lucía
authors.initials: L
authors.lastname: Pérez-Alvarez
authors.forename: Evelyn Yayra
authors.initials: EY
authors.lastname: Bonney
authors.forename: Ya Diul
authors.initials: YD
authors.lastname: Mukadi
authors.forename: Margaret
authors.initials: M
authors.lastname: Lartey
authors.forename: Charles
authors.initials: C
authors.lastname: Nyarko
authors.forename: Richard Noamesi
authors.initials: RN
authors.lastname: Amenyah
authors.forename: Michael
authors.initials: M
authors.lastname: Thomson
authors.forename: Rafael
authors.initials: R
authors.lastname: Nájera
mesh_terms: D019380:Anti-HIV Agents / Q000494:pharmacology*; D024882:Drug Resistance, Viral / Q000235:genetics*; D015751:Genes, pol; D005869:Ghana / Q000453:epidemiology; D015658:HIV Infections / Q000453:epidemiology* / Q000821:virology; D017320:HIV Protease Inhibitors / Q000494:pharmacology; D015497:HIV-1 / Q000145:classification / Q000187:drug effects / Q000235:genetics* / Q000302:isolation & purification; D006801:Humans; D017720:Molecular Epidemiology; D008969:Molecular Sequence Data; D009154:Mutation; D010802:Phylogeny; D011110:Polymorphism, Genetic; D015995:Prevalence; D011995:Recombination, Genetic; D018894:Reverse Transcriptase Inhibitors / Q000494:pharmacology
chemical_list: D019380:Anti-HIV Agents; D017320:HIV Protease Inhibitors; D018894:Reverse Transcriptase Inhibitors