title: Kinetics of plasma cytokines and chemokines during primary HIV-1 infection and after analytical treatment interruption.
abstract: BACKGROUND
  There are strong theoretical arguments for initiating antiretroviral therapy (ART) during primary HIV-1 infection (PHI) to preserve HIV-1-specific T-cell responses and to decrease immune activation.
  
  
  METHODS
  We assessed the degree of immune activation during PHI and after analytical treatment interruption (ATI) in plasma samples from 22 subjects by measuring 13 cytokines/chemokines with the Luminex system. Subjects initiated quadruple ART at PHI (the QUEST cohort) and were classified as responders or nonresponders according to their HIV-1 viral load (VL) 6 months post-ATI.
  
  
  RESULTS
  During PHI, nonresponders had higher levels of HIV-1 RNA, interferon (IFN)-gamma, tumour necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-10 and eotaxin than responders (P</=0.05). A positive correlation was found between VL and IFN-alpha, TNF-alpha, IL-1beta, macrophage inflammatory protein (MIP)-1alpha and MIP-1beta, respectively. Post ATI, responders had higher levels of IFN-gamma, MIP-1beta and monocyte chemotactic protein (MCP)-1 than nonresponders, while nonresponders had higher levels of HIV-1 RNA, IL-15 and eotaxin. Cytokine/chemokine levels were higher during PHI than post-ATI.
  
  
  CONCLUSIONS
  High levels of immune activation during PHI are associated with a worse virological outcome post-ATI. In contrast, VL post-ATI is negatively correlated with IFN-gamma and chemokines. Therefore, the degree of immune activation during PHI is associated with both the VL at PHI and the viral set-point post-ART.
authors.affiliation: Department of Laboratory Medicine, Division of Clinical Virology, Stockholm, Sweden. babilonia.barqasho@ki.se
authors.forename: B
authors.initials: B
authors.lastname: Barqasho
authors.forename: P
authors.initials: P
authors.lastname: Nowak
authors.forename: A
authors.initials: A
authors.lastname: Tjernlund
authors.forename: S
authors.initials: S
authors.lastname: Kinloch
authors.forename: L-E
authors.initials: LE
authors.lastname: Goh
authors.forename: F
authors.initials: F
authors.lastname: Lampe
authors.forename: M
authors.initials: M
authors.lastname: Fisher
authors.forename: J
authors.initials: J
authors.lastname: Andersson
authors.forename: A
authors.initials: A
authors.lastname: Sönnerborg
mesh_terms: D023241:Antiretroviral Therapy, Highly Active / Q000379:methods; D018791:CD4 Lymphocyte Count; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology*; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology*; D016207:Cytokines / Q000276:immunology*; D005260:Female; D015658:HIV Infections / Q000188:drug therapy / Q000276:immunology*; D015497:HIV-1 / Q000276:immunology*; D006801:Humans; D007155:Immunologic Factors / Q000276:immunology; D008297:Male; D008875:Middle Aged; D019562:Viral Load; D028761:Withholding Treatment
chemical_list: D016207:Cytokines; D007155:Immunologic Factors