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Microbial translocation induces persistent macrophage activation unrelated to HIV-1 levels or T-cell activation following therapy.

Publication ,  Journal Article
Wallet, MA; Rodriguez, CA; Yin, L; Saporta, S; Chinratanapisit, S; Hou, W; Sleasman, JW; Goodenow, MM
Published in: AIDS
June 1, 2010

OBJECTIVE: HIV-1 replication and microbial translocation occur concomitant with systemic immune activation. This study delineates mechanisms of immune activation and CD4 T-cell decline in pediatric HIV-1 infection. DESIGN: Cross-sectional and longitudinal cellular and soluble plasma markers for inflammation were evaluated in 14 healthy and 33 perinatally HIV-1-infected pediatric study volunteers prior to and over 96 weeks of protease-inhibitor-containing combination antiretroviral therapy (ART). All HIV-1-infected patients reconstituted CD4 T cells either with suppression of viremia or rebound of drug-resistant virus. METHODS: Systemic immune activation was determined by polychromatic flow cytometry of blood lymphocytes and ELISA for plasma soluble CD27, soluble CD14, and tumor necrosis factor. Microbial translocation was evaluated by limulus amebocyte lysate assay to detect bacterial lipopolysaccharide (LPS) and ELISA for antiendotoxin core antigen immunoglobulin M (IgM) antibodies. Immune activation markers were compared with viral load, CD4 cell percentage, and LPS by regression models. Comparisons between healthy and HIV-1-infected or between different viral outcome groups were performed by nonparametric rank sum. RESULTS: Microbial translocation was detected in healthy infants but resolved with age (P < 0.05). LPS and soluble CD14 levels were elevated in all HIV-1-infected patients (P < 0.05 and P < 0.0001, respectively) and persisted even if CD4 T cells were fully reconstituted, virus optimally suppressed, and lymphocyte activation resolved by ART. Children with CD4 T-cell reconstitution but viral rebound following ART continued to display high levels of soluble CD27. CONCLUSION: Microbial translocation in pediatric HIV-1 infection is associated with persistent monocyte/macrophage activation independent of viral replication or T-cell activation.

Duke Scholars

Published In

AIDS

DOI

EISSN

1473-5571

Publication Date

June 1, 2010

Volume

24

Issue

9

Start / End Page

1281 / 1290

Location

England

Related Subject Headings

  • Virus Replication
  • Virology
  • Viral Load
  • Tumor Necrosis Factor-alpha
  • Tumor Necrosis Factor Receptor Superfamily, Member 7
  • Male
  • Macrophage Activation
  • Lipopolysaccharide Receptors
  • Infant
  • Humans
 

Citation

APA
Chicago
ICMJE
MLA
NLM
Wallet, M. A., Rodriguez, C. A., Yin, L., Saporta, S., Chinratanapisit, S., Hou, W., … Goodenow, M. M. (2010). Microbial translocation induces persistent macrophage activation unrelated to HIV-1 levels or T-cell activation following therapy. AIDS, 24(9), 1281–1290. https://doi.org/10.1097/QAD.0b013e328339e228
Wallet, Mark A., Carina A. Rodriguez, Li Yin, Sara Saporta, Sasawan Chinratanapisit, Wei Hou, John W. Sleasman, and Maureen M. Goodenow. “Microbial translocation induces persistent macrophage activation unrelated to HIV-1 levels or T-cell activation following therapy.AIDS 24, no. 9 (June 1, 2010): 1281–90. https://doi.org/10.1097/QAD.0b013e328339e228.
Wallet MA, Rodriguez CA, Yin L, Saporta S, Chinratanapisit S, Hou W, et al. Microbial translocation induces persistent macrophage activation unrelated to HIV-1 levels or T-cell activation following therapy. AIDS. 2010 Jun 1;24(9):1281–90.
Wallet, Mark A., et al. “Microbial translocation induces persistent macrophage activation unrelated to HIV-1 levels or T-cell activation following therapy.AIDS, vol. 24, no. 9, June 2010, pp. 1281–90. Pubmed, doi:10.1097/QAD.0b013e328339e228.
Wallet MA, Rodriguez CA, Yin L, Saporta S, Chinratanapisit S, Hou W, Sleasman JW, Goodenow MM. Microbial translocation induces persistent macrophage activation unrelated to HIV-1 levels or T-cell activation following therapy. AIDS. 2010 Jun 1;24(9):1281–1290.

Published In

AIDS

DOI

EISSN

1473-5571

Publication Date

June 1, 2010

Volume

24

Issue

9

Start / End Page

1281 / 1290

Location

England

Related Subject Headings

  • Virus Replication
  • Virology
  • Viral Load
  • Tumor Necrosis Factor-alpha
  • Tumor Necrosis Factor Receptor Superfamily, Member 7
  • Male
  • Macrophage Activation
  • Lipopolysaccharide Receptors
  • Infant
  • Humans