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Søren Kragh Moestrup

Plasma Soluble CD163 Level Independently Predicts All-Cause Mortality in HIV-1-Infected Individuals

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  • Troels Bygum Knudsen, University of Copenhagen, Denmark
  • Gideon Ertner
  • ,
  • Janne Petersen, University of Copenhagen
  • ,
  • Holger Jon Møller
  • Søren Kragh Moestrup
  • Jesper Eugen-Olsen, Denmark
  • Gitte Kronborg, University of Copenhagen, Denmark
  • Thomas Benfield, University of Copenhagen, Denmark
BACKGROUND: CD163, a monocyte- and macrophage-specific scavenger receptor, is shed as soluble CD163 (sCD163) during the proinflammatory response. Here, we assessed the association between plasma sCD163 levels and progression to AIDS and all-cause mortality among individuals infected with human immunodeficiency virus type 1 (HIV). METHODS: Plasma sCD163 levels were measured in 933 HIV-infected individuals. Hazard ratios (HRs) with 95% confidence intervals (CIs) associated with mortality were computed by Cox proportional hazards regression. RESULTS: At baseline, 86% were receiving antiretroviral treatment, 73% had plasma a HIV RNA level of <50 copies/mL, and the median CD4(+) T-cell count was 503 cells/µL. During 10.5 years of follow-up, 167 (17.9%) died. Plasma sCD163 levels were higher in nonsurvivors than in survivors (4.92 mg/L [interquartile range {IQR}, 3.29-8.65 mg/L] vs 3.16 mg/L [IQR, 2.16-4.64 mg/L]; P = .0001). The cumulative incidence of death increased with increasing plasma sCD163 levels, corresponding to a 6% or 35% increased risk of death for each milligram per liter or quartile increase, respectively, in baseline plasma sCD163 level (adjusted HR, 1.06 [95% CI, 1.03-1.09] and 1.35 [95% CI, 1.13-1.63], respectively). CONCLUSIONS: Plasma sCD163 was an independent marker of all-cause mortality in a cohort of HIV-infected individuals, suggesting that monocyte/macrophage activation may play a role in HIV pathogenesis and be a target of intervention.
Original languageDanish
JournalJournal of Infectious Diseases
Pages (from-to)1198-204
Number of pages7
Publication statusPublished - 15 Oct 2016

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