title: Documented prevalence of HIV type 1 antiretroviral transmitted drug resistance in Ireland from 2004 to 2008.
abstract: HIV-1-infected individuals with transmitted HIV drug resistance (TDR) begin antiretroviral therapy (ART) with a lower genetic barrier to resistance and a higher risk of both virological failure and of developing further resistance. TDR surveillance informs HIV-1 public health strategies and first line ART. TDR has not been studied nationally in an Irish population. This study includes all new HIV diagnoses from January 2004 to September 2008 from the National Virus Reference Laboratory, University College Dublin. HIV-1 protease and reverse transcriptase sequences were generated, and resistance mutations identified using the Siemens TRUGENE HIV-1 Genotyping System. Subtypes were determined using web-based genotyping tools. The study comprised 1579 patients. There were 305 new diagnoses in 2004 (173 male; 132 female), 298 in 2005 (175M; 123F), 321 in 2006 (197M; 124F), 297 in 2007 (184M; 113F), and 358 (235M; 123F) in 2008. HIV-1 RNA was sequenced from 158/305 patients in 2004, 199/298 in 2005, 225/321 in 2006, 203/297 in 2007, and 275/358 in 2008. The overall TDR rate was 6.3%, peaking in 2006 at 10.4% and declining to 5.3% in 2008. The majority of TDR was seen in Irish born individuals with HIV-1 subtype B infection. The TDR rate in Ireland is comparatively low. Thus, a health technology assessment is required to ascertain the most cost effective use of genotypic antiretroviral resistance testing (GART) in the future: the current approach of performing baseline GART on all new diagnoses, or perhaps a more targeted approach that focuses on patients commencing nonnucleoside reverse transcriptase inhibitor (NNRTI)-based ART.
authors.affiliation: National Virus Reference Laboratory, University College Dublin, Dublin, Ireland. cillian.degascun@ucd.ie
authors.forename: Cillian F
authors.initials: CF
authors.lastname: De Gascun
authors.forename: Allison
authors.initials: A
authors.lastname: Waters
authors.forename: Ciara
authors.initials: C
authors.lastname: Regan
authors.forename: Jane
authors.initials: J
authors.lastname: O'Halloran
authors.forename: Gillian
authors.initials: G
authors.lastname: Farrell
authors.forename: Suzie
authors.initials: S
authors.lastname: Coughlan
authors.forename: Colm
authors.initials: C
authors.lastname: Bergin
authors.forename: William G
authors.initials: WG
authors.lastname: Powderly
authors.forename: William W
authors.initials: WW
authors.lastname: Hall
mesh_terms: D000328:Adult; D019380:Anti-HIV Agents / Q000494:pharmacology / Q000627:therapeutic use*; D024882:Drug Resistance, Viral / Q000187:drug effects* / Q000235:genetics; D005260:Female; D005838:Genotype; D016333:HIV Protease / Q000235:genetics; D054303:HIV Reverse Transcriptase / Q000235:genetics; D006679:HIV Seropositivity / Q000188:drug therapy / Q000453:epidemiology* / Q000235:genetics; D015497:HIV-1 / Q000235:genetics / Q000302:isolation & purification*; D006801:Humans; D007494:Ireland / Q000453:epidemiology; D008297:Male; D009154:Mutation / Q000187:drug effects* / Q000235:genetics; D010802:Phylogeny; D015995:Prevalence; D011634:Public Health; D012367:RNA, Viral / Q000097:blood / Q000302:isolation & purification; D018571:Sentinel Surveillance; D017423:Sequence Analysis, RNA
chemical_list: D019380:Anti-HIV Agents; D012367:RNA, Viral; C514824:reverse transcriptase, Human immunodeficiency virus 1; D054303:HIV Reverse Transcriptase; D016333:HIV Protease; C514803:p16 protease, Human immunodeficiency virus 1