title: Virological rebound after suppression on highly active antiretroviral therapy.
abstract: OBJECTIVE To determine the rate of virological rebound and factors associated with rebound among patients on highly active antiretroviral therapy (HAART) with previously undetectable levels of viraemia. DESIGN An observational cohort study of 2444 patients from the EuroSIDA study. METHODS Patients were followed from their first viral load under 400 copies/ml to the first of two consecutive viral loads above 400 copies/ml. Incidence rates were calculated using person-years of follow-up (PYFU), Cox proportional hazards models were used to determine factors related to rebound. RESULTS Of 2444 patients, 1031 experienced virological rebound (42.2%). The incidence of rebound decreased over time; from 33.5 in the first 6 months after initial suppression to 8.6 per 100 PYFU at 2 years after initial suppression (P < 0.0001). The rate of rebound was lower for treatment-naive compared with treatment-experienced patients. In multivariate models, patients who changed treatment were more likely to rebound, as were patients with higher viral loads on starting HAART. Treatment-naive patients were less likely to rebound. Among pretreated patients, those who were started on new nucleosides were less likely to rebound. CONCLUSION The rate of virological rebound decreased over time, suggesting that the greatest risk of treatment failure is in the months after initial suppression. Treatment-naive patients were at a lower risk of rebound, but among drug-experienced patients, those who added new nucleosides had a lower risk of rebound, as were patients with a good immunological response.
authors.affiliation: Royal Free Centre for HIV Medicine and Department of Primary Care and Population Sciences, Royal Free and University College Medical School, London, UK. a.mocroft@pcps.ucl.ac.uk
authors.forename: Amanda
authors.initials: A
authors.lastname: Mocroft
authors.forename: Lidia
authors.initials: L
authors.lastname: Ruiz
authors.forename: Peter
authors.initials: P
authors.lastname: Reiss
authors.forename: Bruno
authors.initials: B
authors.lastname: Ledergerber
authors.forename: Christine
authors.initials: C
authors.lastname: Katlama
authors.forename: Adriano
authors.initials: A
authors.lastname: Lazzarin
authors.forename: Frank-Detlef
authors.initials: FD
authors.lastname: Goebel
authors.forename: Andrew N
authors.initials: AN
authors.lastname: Phillips
authors.forename: Bonaventura
authors.initials: B
authors.lastname: Clotet
authors.forename: Jens D
authors.initials: JD
authors.lastname: Lundgren
mesh_terms: D000328:Adult; D019380:Anti-HIV Agents / Q000627:therapeutic use*; D023241:Antiretroviral Therapy, Highly Active; D004334:Drug Administration Schedule; D005060:Europe; D005260:Female; D005500:Follow-Up Studies; D015658:HIV Infections / Q000188:drug therapy* / Q000821:virology; D017320:HIV Protease Inhibitors / Q000627:therapeutic use; D015497:HIV-1 / Q000502:physiology*; D006801:Humans; D019469:Indinavir / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D016016:Proportional Hazards Models; D011446:Prospective Studies; D018894:Reverse Transcriptase Inhibitors / Q000627:therapeutic use; D019438:Ritonavir / Q000627:therapeutic use; D019258:Saquinavir / Q000627:therapeutic use; D017211:Treatment Failure; D019562:Viral Load; D014766:Viremia
chemical_list: D019380:Anti-HIV Agents; D017320:HIV Protease Inhibitors; D018894:Reverse Transcriptase Inhibitors; D019469:Indinavir; D019258:Saquinavir; D019438:Ritonavir