Abstract
BackgroundAssessing whether hepatitis C (HCV) co-infection with human immunodeficiency virus (HIV) is associated with increased inflammation is complex. The liver, integral to inflammatory biomarker synthesis, is compromised by HCV and alcohol abuse. Using single liver-synthesized biomarkers (e.g. C-reactive protein) to represent inflammation may not be appropriate in HIV/HCV co-infection. We hypothesized that 1) detectable HIV/HCV RNA was independently associated with increased inflammation; 2) a composite inflammation measure describes inflammation differently from single inflammatory biomarkers.MethodsWe compared inflammation by HIV/HCV group in a cohort of 361 HIV infected participants from the HIV-Longitudinal Interrelationships of Viruses and Ethanol study. Inflammatory biomarkers >75th percentile were considered elevated. Associations between HIV/HCV group and elevated biomarkers were analyzed as a composite measure (inflammatory burden) or individually. We defined inflammatory burden as number of concurrently elevated biomarkers. Biomarkers included interleukin-6 (IL-6), C-reactive protein (CRP), cystatin C, serum amyloid-A (SAA), tumor necrosis factor-alpha (TNF-α), interleukin-10 (IL-10). Covariates: alcohol, liver fibrosis, comorbidities, CD4 count, antiretroviral therapy, substance use.ResultsDetectable HIV and HCV RNA (OR = 2.49; 95% CI = 1.05–5.89) and detectable HCV RNA alone (2.95; 1.08–8.01) were independently associated with increased odds of having a greater inflammatory burden compared to undetectable viremia. Elevated IL-10 (7.79; 1.90–31.97) and TNF-α (7.70; 1.42–41.83) were independently associated with detectable HIV and HCV RNA. Elevated IL-10 was also associated with detectable HCV RNA alone (5.51; 1.17, 25.84).ConclusionsDetectable HIV and HCV replication versus undetectable replication was associated with inflammatory burden and certain inflammatory biomarkers independently of alcohol consumption, liver fibrosis and other comorbidities.
Highlights
Assessing whether hepatitis C (HCV) co-infection with human immunodeficiency virus (HIV) is associated with increased inflammation is complex
Several reports suggest that human immunodeficiency virus (HIV) infection and hepatitis C (HCV) co-infection with HIV are associated with increased cardiovascular disease (CVD) risk [1,2,3,4]
Liver damage caused by alcohol consumption and HCV may alter serum levels of inflammatory biomarkers that are synthesized in the liver (e.g., C reactive protein) and possibly confound the association between viremia and biomarkers of systemic inflammation
Summary
Assessing whether hepatitis C (HCV) co-infection with human immunodeficiency virus (HIV) is associated with increased inflammation is complex. Using single liver-synthesized biomarkers (e.g. C-reactive protein) to represent inflammation may not be appropriate in HIV/HCV co-infection. Several reports suggest that human immunodeficiency virus (HIV) infection and hepatitis C (HCV) co-infection with HIV are associated with increased cardiovascular disease (CVD) risk [1,2,3,4]. Liver damage caused by alcohol consumption and HCV may alter serum levels of inflammatory biomarkers that are synthesized in the liver (e.g., C reactive protein) and possibly confound the association between viremia and biomarkers of systemic inflammation. Whether a composite measure involving multiple elevated inflammatory biomarkers, including those synthesized in the liver, provides a more complete representation of the state of inflammation in the setting of HIV/HCV infection is not clear
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