title: C-reactive protein levels increase during HIV-1 disease progression in Rakai, Uganda, despite the absence of microbial translocation.
abstract: BACKGROUND
  Microbial translocation has been implicated as a contributing factor to the heightened immune activation observed during HIV-1 disease progression. When examined in a longitudinal study of HIV-1 seroconverters in Rakai, Uganda, microbial translocation was not associated with HIV-1 disease progression. However, the role of general immune activation in HIV disease progression in this population was not fully examined.
  
  
  METHODS
  Longitudinal serum samples of HIV-1 seroconverters in three HIV-1 disease progression groups [long-term nonprogressors (LTNP), standard progressors (SP), and rapid progressors (RP)] from Rakai, Uganda, were tested for levels of C-reactive protein (CRP), a marker for immune activation.
  
  
  RESULTS
  CRP levels significantly increased in the SP group (P < 0.0001) but not in the RP group or the LTNP group. CRP levels during the first year post-HIV seroconversion in the RP group were significantly higher than those observed in the LTNP group (P < 0.05). For the entire population, CRP levels negatively correlated with lipopolysaccharide levels (P < 0.05) and were not associated with endotoxin antibody levels.
  
  
  CONCLUSIONS
  This study suggests that in this population, increased immune activation is significantly associated with HIV-1 disease progression but not microbial translocation.
authors.affiliation: Laboratory of Immunoregulation, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.
authors.forename: Andrew D
authors.initials: AD
authors.lastname: Redd
authors.forename: Kevin P
authors.initials: KP
authors.lastname: Eaton
authors.forename: Xiangrong
authors.initials: X
authors.lastname: Kong
authors.forename: Oliver
authors.initials: O
authors.lastname: Laeyendecker
authors.forename: Tom
authors.initials: T
authors.lastname: Lutalo
authors.forename: Maria J
authors.initials: MJ
authors.lastname: Wawer
authors.forename: Ronald H
authors.initials: RH
authors.lastname: Gray
authors.forename: David
authors.initials: D
authors.lastname: Serwadda
authors.forename: Thomas C
authors.initials: TC
authors.lastname: Quinn
mesh_terms: D001774:Blood Chemical Analysis; D002097:C-Reactive Protein / Q000032:analysis*; D018450:Disease Progression; D015658:HIV Infections / Q000276:immunology* / Q000473:pathology* / Q000821:virology; D015497:HIV-1 / Q000276:immunology* / Q000302:isolation & purification; D006801:Humans; D008137:Longitudinal Studies; D014454:Uganda
chemical_list: D002097:C-Reactive Protein
references.citation: Nat Med. 2006 Dec;12(12):1365-71
references.pmid: 17115046
references.citation: BMC Infect Dis. 2008 Nov 13;8:156
references.pmid: 19014537
references.citation: Nutrition. 1999 Nov-Dec;15(11-12):865-9
references.pmid: 10575662
references.citation: Nature. 2001 Apr 19;410(6831):974-9
references.pmid: 11309627
references.citation: AIDS Rev. 2003 Jul-Sep;5(3):172-7
references.pmid: 14598566
references.citation: Immunol Today. 1995 Apr;16(4):187-91
references.pmid: 7734046
references.citation: Arch Intern Med. 2006 Jan 9;166(1):64-70
references.pmid: 16401812
references.citation: AIDS. 1996 Nov;10(13):1535-42
references.pmid: 8931789
references.citation: J Clin Invest. 2003 Jun;111(12):1805-12
references.pmid: 12813013
references.citation: Nat Immunol. 2006 Mar;7(3):235-9
references.pmid: 16482171
references.citation: AIDS. 2007 Oct 1;21(15):2067-75
references.pmid: 17885297
references.citation: Proc Natl Acad Sci U S A. 2009 Apr 21;106(16):6718-23
references.pmid: 19357303