title: Slower decline of plasma HIV-1 RNA following highly suppressive antiretroviral therapy in primary compared with chronic infection.
abstract: OBJECTIVE
  To study the effect of highly suppressive antiretroviral therapy on the slopes of HIV-1 RNA decline in primary compared with chronic HIV-1 infection.
  
  
  METHODS
  Slopes of HIV-1 RNA decline in plasma were compared before and after the start of highly suppressive antiretroviral therapy from five acutely infected patients who started treatment 2 to 5 weeks following the onset of clinical symptoms. Slopes of decline after the initiation of therapy were also compared with those found in 12 chronically infected individuals on the same therapy. Numbers and percentages of activated CD4 and CD8 T cells at baseline were compared as well.
  
  
  RESULTS
  The pre-treatment slopes of HIV-1 RNA decline in the acutely infected individuals increased significantly (P = 0.0001) after the start of anti-retroviral therapy. However, these post-treatment slopes were lower than those found in the chronically infected individuals (P= 0.012). Slopes were inversely correlated (P= 0.012) with baseline HIV-1 RNA. Although the number of CD38+HLA-DR+ CD4 cells was higher in primary infection (P= 0.02), the percentage did not differ between primary and chronic infection.
  
  
  CONCLUSIONS
  These findings indicate that antiretroviral therapy contributes significantly to the clearance of HIV-1 during primary infection. Based on the mathematical model the less steep RNA slope following the start of treatment in primary infection can be predicted to be the result of lower clearance of productively infected cells and higher burst size per cell per unit time. This may indicate a growing immune response to HIV-1 in this very early stage of infection.
authors.affiliation: Department of Human Retrovirology, University of Amsterdam, The Netherlands.
authors.forename: H
authors.initials: H
authors.lastname: Putter
authors.forename: J M
authors.initials: JM
authors.lastname: Prins
authors.forename: S
authors.initials: S
authors.lastname: Jurriaans
authors.forename: M
authors.initials: M
authors.lastname: Roos
authors.forename: N M
authors.initials: NM
authors.lastname: Ferguson
authors.forename: R
authors.initials: R
authors.lastname: van Praag
authors.forename: L
authors.initials: L
authors.lastname: van der Hoek
authors.forename: H
authors.initials: H
authors.lastname: Schuitemaker
authors.forename: R M
authors.initials: RM
authors.lastname: Anderson
authors.forename: J
authors.initials: J
authors.lastname: Goudsmit
authors.forename: J M
authors.initials: JM
authors.lastname: Lange
authors.forename: F
authors.initials: F
authors.lastname: de Wolf
mesh_terms: D000208:Acute Disease; D000328:Adult; D019380:Anti-HIV Agents / Q000627:therapeutic use*; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology; D002908:Chronic Disease; D004359:Drug Therapy, Combination; D015658:HIV Infections / Q000188:drug therapy / Q000276:immunology / Q000821:virology*; D015497:HIV-1 / Q000502:physiology*; D006801:Humans; D008213:Lymphocyte Activation; D008297:Male; D008875:Middle Aged; D012367:RNA, Viral / Q000097:blood*; D018894:Reverse Transcriptase Inhibitors / Q000627:therapeutic use*; D019562:Viral Load
chemical_list: D019380:Anti-HIV Agents; D012367:RNA, Viral; D018894:Reverse Transcriptase Inhibitors