|Low-level HIV viremia is associated with microbial translocation and inflammation.|
|PMID: 23018379 Owner: NLM Status: MEDLINE|
|BACKGROUND: Decrease in HIV viral load (VL) is accompanied by decrease in microbial translocation (MT) and chronic inflammation, but the behavior of these markers in patients with HIV-VL <20 copies per milliliter is unknown. The aim of this study was to determine whether strict control of HIV-VL is associated with MT and chronic inflammation.
METHODS: Observational cross-sectional study. Inclusion criteria: HIV patients receiving antiretroviral therapy and HIV-VL <200 copies per milliliter for more than 6 months. Exclusion criteria: chronic liver disease, active infection, or antibiotic consumption. Recruitment: patients who consecutively visited the outpatient clinic in November 2011. Primary endpoint: molecular MT as determined by detection in plasma of 16S ribosomal DNA. Secondary variables: lipopolysaccharide, soluble CD14, tumor necrosis factor α, and interleukin 6. Primary explanatory variable: HIV-VL (COBAS AmpliPrep/COBAS TaqMan HIV-1 test, version 2.0) with a detection limit of 20 copies per milliliter.
RESULTS: Fifty-two patients were included: 65% men, median age 45 years, HIV acquired predominantly through sex (75%), 40% Centers for Disease Control and Prevention stage C, and median CD4 lymphocyte count 552 cells per cubic millimeter (range, 126-1640 cells/mm). Molecular MT was observed in 46% and 18% of patients with low-level (20-200 copies/mL) and negative (<20 copies/mL) HIV-VL, respectively (P < 0.05). Plasma levels of inflammatory markers (tumor necrosis factor α and interleukin 6) were higher in patients with molecular MT (P < 0.01) and were not influenced for HIV-VL.
CONCLUSIONS: Patients with HIV infection receiving treatment and negative HIV-VL (<20 copies/mL) present less frequently MT than patients with low-level HIV viremias (20-200 copies/mL). MT is associated with higher levels of inflammation markers, independent of HIV-VL.
|Sergio Reus; Joaquín Portilla; José Sánchez-Payá; Livia Giner; Rubén Francés; José Such; Vicente Boix; Esperanza Merino; Adelina Gimeno|
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|Type: Journal Article; Research Support, Non-U.S. Gov't|
|Title: Journal of acquired immune deficiency syndromes (1999) Volume: 62 ISSN: 1944-7884 ISO Abbreviation: J. Acquir. Immune Defic. Syndr. Publication Date: 2013 Feb|
|Created Date: 2013-01-18 Completed Date: 2013-03-08 Revised Date: 2013-03-27|
Medline Journal Info:
|Nlm Unique ID: 100892005 Medline TA: J Acquir Immune Defic Syndr Country: United States|
|Languages: eng Pagination: 129-34 Citation Subset: IM; X|
|Infectious Disease Unit , Hospital General Universitario de Alicante, Alicante, Spain. email@example.com|
|APA/MLA Format Download EndNote Download BibTex|
Anti-Retroviral Agents / therapeutic use
Antigens, CD14 / blood
Biological Markers / blood
CD4 Lymphocyte Count
DNA, Bacterial / blood
DNA, Ribosomal / blood
HIV Infections / drug therapy, immunology, virology*
Inflammation / blood*, complications, virology
Interleukin-6 / blood
Lipopolysaccharides / blood
Ribosomal Proteins / genetics
Tumor Necrosis Factor-alpha / blood
Viremia / complications, virology*
|0/Anti-Retroviral Agents; 0/Antigens, CD14; 0/Biological Markers; 0/DNA, Bacterial; 0/DNA, Ribosomal; 0/Interleukin-6; 0/Lipopolysaccharides; 0/Ribosomal Proteins; 0/Rps16 protein, human; 0/Tumor Necrosis Factor-alpha|
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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