PMID- 24378729 OWN - NLM STAT- MEDLINE DCOM- 20140602 LR - 20211021 IS - 1944-7884 (Electronic) IS - 1525-4135 (Print) IS - 1525-4135 (Linking) VI - 66 IP - 1 DP - 2014 May 1 TI - Immune activation is associated with increased gut microbial translocation in treatment-naive, HIV-infected children in a resource-limited setting. PG - 16-24 LID - 10.1097/QAI.0000000000000096 [doi] AB - BACKGROUND: Gut damage resulting in microbial translocation (MT) is considered a major cause of immune activation (IA) in HIV infection, but data in children are limited, particularly in the absence of antiretroviral therapy. METHODS: Sixty perinatally HIV-infected, antiretroviral therapy-naive children, aged 2-12 years, were evaluated for plasma levels of lipopolysaccharide, DNA sequences encoding bacterial 16 second ribosomal DNA (16S rDNA) and soluble CD14 concurrently with markers of CD4 and CD8 T-cell IA and immune exhaustion (IE), CD4 counts, and plasma viral load. At study entry, participants were classified into immune categories (ICs): IC1 (CD4% > 25), IC2 (CD4% 15-25), and IC3 (CD4% < 15). Age-matched HIV-uninfected children served as controls. Data were evaluated at study entry and at 12 months. RESULTS: Levels of MT, IA, and IE were increased in patients as compared with controls, were highest in patients in IC3 group, and did not change over 12 months. MT products lipopolysaccharide and 16S rDNA correlated with each other and each correlated with plasma viral load, soluble CD14, and T-cell IA and IE. There was a correlation of IA with IE. CD4 counts and percentage were inversely correlated with MT products and underlying CD4 activation. CONCLUSIONS: In a natural history cohort of HIV-infected children not on therapy, MT was more pronounced in the most severely immunocompromised patients and was associated with IA. Strategies to reduce MT may help to reduce IA and prevent CD4 depletion. FAU - Pilakka-Kanthikeel, Sudheesh AU - Pilakka-Kanthikeel S AD - *Department of Microbiology and Immunology, Miami Center for AIDS Research, University of Miami Miller School of Medicine, Miami, FL; daggerDepartment of Public Health Sciences, Division of Biostatistics, University of Miami Miller School of Medicine, Miami, FL; and double daggerDepartment of Clinical Research, Tuberculosis Research Center, Indian Council of Medical Research, Chennai, India (Sudheesh Pilakka-Kanthikeel is now with the Department of Immunology, Herbert-Wertheim College of Medicine, Florida International University, Miami, FL). FAU - Kris, Arheart AU - Kris A FAU - Selvaraj, Anbalagan AU - Selvaraj A FAU - Swaminathan, Soumya AU - Swaminathan S FAU - Pahwa, Savita AU - Pahwa S LA - eng GR - P30 AI073961/AI/NIAID NIH HHS/United States GR - R03 HD052154/HD/NICHD NIH HHS/United States GR - R03-HD052154-01/HD/NICHD NIH HHS/United States PT - Journal Article PT - Research Support, N.I.H., Extramural PT - Research Support, Non-U.S. Gov't PL - United States TA - J Acquir Immune Defic Syndr JT - Journal of acquired immune deficiency syndromes (1999) JID - 100892005 RN - 0 (DNA, Bacterial) RN - 0 (DNA, Ribosomal) RN - 0 (Lipopolysaccharide Receptors) RN - 0 (Lipopolysaccharides) SB - IM MH - Adolescent MH - *Bacterial Translocation MH - CD4 Lymphocyte Count MH - CD4-Positive T-Lymphocytes/immunology MH - CD8-Positive T-Lymphocytes/immunology MH - Child MH - Child, Preschool MH - DNA, Bacterial/blood MH - DNA, Ribosomal/blood MH - Female MH - Gastrointestinal Tract/*immunology/*physiopathology MH - HIV Infections/*complications/*immunology/pathology MH - Humans MH - Infant MH - Lipopolysaccharide Receptors/blood MH - Lipopolysaccharides/blood MH - Male MH - Viral Load PMC - PMC4386670 MID - NIHMS558607 EDAT- 2014/01/01 06:00 MHDA- 2014/06/03 06:00 PMCR- 2015/05/01 CRDT- 2014/01/01 06:00 PHST- 2014/01/01 06:00 [entrez] PHST- 2014/01/01 06:00 [pubmed] PHST- 2014/06/03 06:00 [medline] PHST- 2015/05/01 00:00 [pmc-release] AID - 10.1097/QAI.0000000000000096 [doi] PST - ppublish SO - J Acquir Immune Defic Syndr. 2014 May 1;66(1):16-24. doi: 10.1097/QAI.0000000000000096.