Effect of chronic hepatitis C virus infection on inflammatory lipid mediators 1

• Published in: Digestive and liver disease Vol. 39; pp. S76 - S82
• Main Authors: Guerra, Cristina Tosti, Caini, Patrizio, Giannini, Carlo, Giannelli, Francesca, Gragnani, Laura, Petrarca, Antonio, Solazzo, Vera, Monti, Monica, Laffi, Giacomo, Zignego, Anna Linda
• Format: Journal Article
• Language: English
• Published: Elsevier Ltd 2007
• Subjects: Gastroenterology and Hepatology; Hepatitis C virus; Plasma PAF-acetylhydrolase; Platelet-activating factor; Hepatitis C virus; Platelet-activating factor; Plasma PAF-acetylhydrolase
• ISSN: 1590-8658; 1878-3562
• DOI: 10.1016/S1590-8658(07)80016-8

Background: Platelet-activating factor (PAF), a powerful phospholipid mediator of inflammation, is degraded by plasma PAF-acetyl-hydxolase (pPAF-AH), an enzyme which circulates in serum mainly in a complex with lipoproteins that confer its biological activity. Hepatitis C virus (HCV) is linked to lipoproteins in serum too. Reduced pPAF-AH activity was observed in several diseases, including systemic vasculitis. Aim: To evaluate if chronic HCV infection could alter pPAF-AH physiological functions. Subjects: 145 subjects were studied: 56 HCV- and 52 HBV-infected patients (pathologic controls); 37 healthy subjects (healthy controls). Methods: pPAF-AH activity, PAF and Apo B100 titers were determined in plasma; enzyme expression levels were evaluated in monocyte-derived macrophages. HCV-RNA was detected in plasma, peripheral blood mononuclear cells and liver samples. Results: HCV-infected patients showed an increase of PAF levels following a significant decrease of pPAF-AH activity. A recovery of pPAF-AH activity occurs only in patients who clear HCV after the antiviral treatment. Expression levels of pPAF-AH mRNA and Apo B100 titers were not modified in HCV patients in comparison to controls. Conclusion: In light of these results, it is tempting to hypothesize that during chronic HCV infection, the PAF/pPAF-AH system may be altered and this condition may contribute to HCV-related vascular damage.