title: Low-level HIV viremia is associated with microbial translocation and inflammation.
abstract: 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.
  
  
  METHODS
  HIV patients receiving antiretroviral therapy and HIV-VL <200 copies per milliliter for more than 6 months.
  
  
  METHODS
  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.
authors.affiliation: Infectious Disease Unit , Hospital General Universitario de Alicante, Alicante, Spain. reus_ser@gva.es
authors.forename: Sergio
authors.initials: S
authors.lastname: Reus
authors.forename: Joaquín
authors.initials: J
authors.lastname: Portilla
authors.forename: José
authors.initials: J
authors.lastname: Sánchez-Payá
authors.forename: Livia
authors.initials: L
authors.lastname: Giner
authors.forename: Rubén
authors.initials: R
authors.lastname: Francés
authors.forename: José
authors.initials: J
authors.lastname: Such
authors.forename: Vicente
authors.initials: V
authors.lastname: Boix
authors.forename: Esperanza
authors.initials: E
authors.lastname: Merino
authors.forename: Adelina
authors.initials: A
authors.lastname: Gimeno
mesh_terms: D000328:Adult; D000368:Aged; D044966:Anti-Retroviral Agents / Q000627:therapeutic use; D018988:Bacterial Translocation; D015415:Biomarkers / Q000097:blood; D018791:CD4 Lymphocyte Count; D016009:Chi-Square Distribution; D002908:Chronic Disease; D003430:Cross-Sectional Studies; D004269:DNA, Bacterial / Q000097:blood; D004275:DNA, Ribosomal / Q000097:blood; D005260:Female; D015658:HIV Infections / Q000188:drug therapy / Q000276:immunology / Q000821:virology*; D006801:Humans; D007249:Inflammation / Q000097:blood* / Q000150:complications / Q000821:virology; D015850:Interleukin-6 / Q000097:blood; D018950:Lipopolysaccharide Receptors / Q000097:blood; D008070:Lipopolysaccharides / Q000097:blood; D008297:Male; D008875:Middle Aged; D012269:Ribosomal Proteins / Q000235:genetics; D012307:Risk Factors; D018709:Statistics, Nonparametric; D014409:Tumor Necrosis Factor-alpha / Q000097:blood; D019562:Viral Load; D014766:Viremia / Q000150:complications / Q000821:virology*; D055815:Young Adult
chemical_list: D044966:Anti-Retroviral Agents; D015415:Biomarkers; D004269:DNA, Bacterial; D004275:DNA, Ribosomal; D015850:Interleukin-6; D018950:Lipopolysaccharide Receptors; D008070:Lipopolysaccharides; D012269:Ribosomal Proteins; C421090:Rps16 protein, human; D014409:Tumor Necrosis Factor-alpha