title: Brief Report: Changes in Levels of Inflammation After Antiretroviral Treatment During Early HIV Infection in AIDS Clinical Trials Group Study A5217.
abstract: We evaluated the changes in the levels of soluble biomarkers of inflammation and coagulation and T-cell activation among participants of AIDS Clinical Trials Group Study A5217 who were started on antiretroviral therapy (ART) within the first 6 months of HIV infection.
  
  
  
  Cryopreserved specimens were obtained pre-ART (week 0), at the time of virologic suppression (week 36), and at 36 weeks after treatment interruption (week 72). Levels of D-dimer, C-reactive protein (CRP), and soluble CD14 (sCD14) were measured in plasma, whereas T-cell activation levels, defined as the frequencies of CD4 and CD8 T cells coexpressing HLA-DR and CD38, were measured in peripheral blood mononuclear cells.
  
  
  
  D-dimer levels were significantly lower at viral suppression (P = 0.031), whereas CRP and sCD14 levels remained similar to pre-ART levels. At viral suppression, levels of the soluble markers did not correlate with each other. CD4 T-cell counts pre-ART tended to modestly correlate with levels of D-dimer (r = 0.35; P = 0.058) and CRP (r = 0.33; P = 0.078). At 36 weeks after treatment interruption (week 72), D-dimer levels returned back to pre-ART levels. However, CD8 T-cell activation was significantly lower than pre-ART levels (35.8% at week 0 vs 28.9% at week 72; P = 0.004).
  
  
  
  Among the A5217 participants who started ART within the first 6 months of HIV infection, high levels of sCD14 and CRP remain similar to pre-ART levels, suggesting that immune damage occurring in the initial stages of infection persists despite short-term virologic suppression.
authors.affiliation: *Department of Medicine, School of Medicine, University of Pittsburgh, Pittsburgh, PA; †Statistical and Data Analysis Center, Harvard T.H. Chan School of Public Health, Boston, MA; ‡Department of Medicine, University of California San Diego, San Diego, CA; §Department of Medicine, Medical College of Wisconsin, Milwaukee, WI; and ‖Department of Infectious Diseases and Microbiology, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA.
authors.forename: Bernard J
authors.initials: BJ
authors.lastname: Macatangay
authors.forename: Ming
authors.initials: M
authors.lastname: Yang
authors.forename: Xin
authors.initials: X
authors.lastname: Sun
authors.forename: Jessica
authors.initials: J
authors.lastname: Morton
authors.forename: Victor
authors.initials: V
authors.lastname: De Gruttola
authors.forename: Susan
authors.initials: S
authors.lastname: Little
authors.forename: Christine
authors.initials: C
authors.lastname: Hogan
authors.forename: Charles R
authors.initials: CR
authors.lastname: Rinaldo
mesh_terms: D051997:ADP-ribosyl Cyclase 1 / Q000032:analysis; D000328:Adult; D044966:Anti-Retroviral Agents / Q000627:therapeutic use*; D015415:Biomarkers / Q000097:blood*; D001777:Blood Coagulation; D002097:C-Reactive Protein / Q000032:analysis; D015496:CD4-Positive T-Lymphocytes / Q000737:chemistry; D018414:CD8-Positive T-Lymphocytes / Q000737:chemistry; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000032:analysis; D015658:HIV Infections / Q000188:drug therapy* / Q000473:pathology*; D006684:HLA-DR Antigens / Q000032:analysis; D006801:Humans; D007249:Inflammation / Q000473:pathology*; D018950:Lipopolysaccharide Receptors / Q000097:blood; D008213:Lymphocyte Activation; D008297:Male; D008562:Membrane Glycoproteins / Q000032:analysis; D010949:Plasma / Q000737:chemistry; D016896:Treatment Outcome
chemical_list: D044966:Anti-Retroviral Agents; D015415:Biomarkers; D005338:Fibrin Fibrinogen Degradation Products; D006684:HLA-DR Antigens; D018950:Lipopolysaccharide Receptors; D008562:Membrane Glycoproteins; C036309:fibrin fragment D; D002097:C-Reactive Protein; C498154:CD38 protein, human; D051997:ADP-ribosyl Cyclase 1