title: Increased microbial translocation in ≤ 180 days old perinatally human immunodeficiency virus-positive infants as compared with human immunodeficiency virus-exposed uninfected infants of similar age.
abstract: BACKGROUND
  The effect of early versus deferred antiretroviral treatment (ART) on plasma concentration of lipopolysaccharide (LPS) and host LPS-binding molecules in human immunodeficiency virus (HIV)-infected infants up to 1 year of age was investigated.
  
  
  METHODS
  We evaluated 54 perinatally HIV-infected and 22 HIV-exposed uninfected infants (controls) at the first and second semester of life. All HIV-infected infants had a baseline CD4 of ≥ 25%, participated in the Comprehensive International Program of Research on AIDS Children with HIV Early Antiretroviral Therapy trial in South Africa, and were randomized in the following groups: group 1 (n = 20), ART deferred until CD4 < 25% or severe HIV disease; and group 2 (n = 34), ART initiation within 6 to 12 weeks of age. LPS, endotoxin-core antibodies, soluble CD14 (sCD14), and LPS-binding protein (LBP) were measured in cryopreserved plasma. T-cell activation was measured in fresh whole blood.
  
  
  RESULTS
  At the first semester, LPS concentration was higher in HIV-infected infants than in controls; sCD14, LBP, and T-cell activation were higher in group 1 than in group 2 and controls. Although LPS was not correlated with study variables, viral load was positively associated with sCD14, LBP, or endotoxin-core antibodies. At the second semester, LPS was not detectable and elevated host LPS-control molecules values were sustained in all groups and in conjunction with ART in all HIV-infected infants.
  
  
  CONCLUSIONS
  Although plasma concentration of LPS was higher in perinatally HIV-infected infants 0 to 6 months of age than in controls independent of ART initiation strategy, concentration of LPS-control molecules was higher in infants with deferred ART, suggesting the presence of increased microbial translocation in HIV-infected infants with sustained early viral replication.
authors.affiliation: The Wistar Institute, Philadelphia, PA, USA.
authors.forename: Emmanouil
authors.initials: E
authors.lastname: Papasavvas
authors.forename: Livio
authors.initials: L
authors.lastname: Azzoni
authors.forename: Andrea
authors.initials: A
authors.lastname: Foulkes
authors.forename: Avy
authors.initials: A
authors.lastname: Violari
authors.forename: Mark F
authors.initials: MF
authors.lastname: Cotton
authors.forename: Maxwell
authors.initials: M
authors.lastname: Pistilli
authors.forename: Griffin
authors.initials: G
authors.lastname: Reynolds
authors.forename: Xiangfan
authors.initials: X
authors.lastname: Yin
authors.forename: Deborah K
authors.initials: DK
authors.lastname: Glencross
authors.forename: Wendy S
authors.initials: WS
authors.lastname: Stevens
authors.forename: James A
authors.initials: JA
authors.lastname: McIntyre
authors.forename: Luis J
authors.initials: LJ
authors.lastname: Montaner
mesh_terms: D019380:Anti-HIV Agents / Q000008:administration & dosage*; D023241:Antiretroviral Therapy, Highly Active / Q000379:methods*; D016470:Bacteremia / Q000175:diagnosis*; D018988:Bacterial Translocation; D006678:HIV / Q000472:pathogenicity; D015658:HIV Infections / Q000150:complications* / Q000188:drug therapy*; D006801:Humans; D007223:Infant; D008070:Lipopolysaccharides / Q000097:blood*; D013019:South Africa; D013997:Time Factors
chemical_list: D019380:Anti-HIV Agents; D008070:Lipopolysaccharides