title: HIV-1 viral rebound dynamics after a single treatment interruption depends on time of initiation of highly active antiretroviral therapy.
abstract: OBJECTIVE
  An important pending question is whether temporary highly active antiretroviral therapy during primary HIV infection can influence viral rebound dynamics and the subsequently established viral setpoint, through preservation and enhancement of HIV-1-specific immune responses, or through other mechanisms.
  
  
  METHODS
  We included all patients from two prospective studies who underwent a single treatment interruption while being well suppressed on highly active antiretroviral therapy. One group started highly active antiretroviral therapy during primary HIV infection, and the other group started it during chronic HIV infection with CD4 cell counts above 350 cells/microl. Data were collected up to 48 weeks from treatment interruption. The median time to viral rebound was analysed for three levels of viraemia: 50, 500 and 5000 copies HIV-RNA/ml plasma.
  
  
  RESULTS
  The median time to viral rebound was significantly longer in primary HIV infection patients (n = 24) than in chronic HIV infection patients (n = 46): 8 versus 4 weeks (P < 0.001 for all three endpoints). In two primary HIV infection patients, no rebound of plasma HIV-1 RNA over 50 copies/ml occurred. In the first 4 weeks after treatment interruption, CD4+ T-cell counts declined with a median of -5.0 cells/microl blood per week in the primary HIV infection group and -45 cells/microl blood per week in the chronic HIV infection group (P < 0.05). From week 4 to 48, the decline in CD4+ T-cell count was similar in both groups.
  
  
  CONCLUSIONS
  Plasma viral load and CD4 dynamics after a single interruption of highly active antiretroviral therapy were different for primary HIV infection and chronic HIV infection patients. Viral rebound is delayed or absent and early CD4 cell count decline after treatment interruption is less pronounced in primary HIV infection patients.
authors.affiliation: Department of Internal Medicine, Division of Infectious Diseases, Tropical Medicine and AIDS, and Center for Infection and Immunity Amsterdam, Academic Medical Center, Amsterdam, The Netherlands. r.steingrover@amc.uva.nl
authors.forename: Radjin
authors.initials: R
authors.lastname: Steingrover
authors.forename: Katalyn
authors.initials: K
authors.lastname: Pogány
authors.forename: Evian
authors.initials: E
authors.lastname: Fernandez Garcia
authors.forename: Suzanne
authors.initials: S
authors.lastname: Jurriaans
authors.forename: Kees
authors.initials: K
authors.lastname: Brinkman
authors.forename: Hanneke
authors.initials: H
authors.lastname: Schuitemaker
authors.forename: Frank
authors.initials: F
authors.lastname: Miedema
authors.forename: Joep Ma
authors.initials: JM
authors.lastname: Lange
authors.forename: Jan M
authors.initials: JM
authors.lastname: Prins
mesh_terms: D000328:Adult; D019380:Anti-HIV Agents / Q000627:therapeutic use*; D023241:Antiretroviral Therapy, Highly Active; D018791:CD4 Lymphocyte Count; D002908:Chronic Disease; D018450:Disease Progression; D004334:Drug Administration Schedule; D005260:Female; D015658:HIV Infections / Q000188:drug therapy* / Q000276:immunology / Q000821:virology*; D015497:HIV-1 / Q000235:genetics / Q000502:physiology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D012367:RNA, Viral / Q000097:blood; D018709:Statistics, Nonparametric; D019562:Viral Load; D014779:Virus Replication
chemical_list: D019380:Anti-HIV Agents; D012367:RNA, Viral