Cytokines and serum amyloid A in the pathogenesis of hepatitis C virus infection. (December 2019)

• Record Type: Journal Article
• Authors: Abouelasrar Salama, Sara; Lavie, Muriel; De Buck, Mieke; Van Damme, Jo; Struyf, Sofie
• Is Part Of: Cytokine & growth factor reviews. Volume 50(2019)
• Page Start: 29
• Page End: 42
• Publication Date: 2019-12
• Subjects: Cytokines -- Serum amyloid A -- Hepatitis C virus -- IL-1 -- IL-6 -- TNF-α; Cytokines -- Periodicals; 571.84
• DOI: 10.1016/j.cytogfr.2019.10.006
• Languages: English
• ISSNs: 1359-6101

Abstract

Graphical abstract: Highlights: SAA displays anti-viral activity against HCV. SAA is upregulated via several cytokines namely IL-1, IL-6 and TNF-α. HCV indirectly upregulates SAA via upregulation of SAA-inducing cytokines. The interplay between SAA, HCV and lipoproteins may influence HCV infectivity. Abstract: Expression of the acute phase protein serum amyloid A (SAA) is dependent on the release of the pro-inflammatory cytokines IL-1, IL-6 and TNF-α during infection and inflammation. Hepatitis C virus (HCV) upregulates SAA-inducing cytokines. In line with this, a segment of chronically infected individuals display increased circulating levels of SAA. SAA has even been proposed to be a potential biomarker to evaluate treatment efficiency and the course of disease. SAA possesses antiviral activity against HCV via direct interaction with the viral particle, but might also divert infectivity through its function as an apolipoprotein. On the other hand, SAA shares inflammatory and angiogenic activity with chemotactic cytokines by activating the G protein-coupled receptor, formyl peptide receptor 2. These latter properties might promote chronic inflammation and hepatic injury. Indeed, up to 80 % of infected individuals develop chronic disease because they cannot completely clear the infection, due to diversion of the immune response. In this review, we summarize the interconnection between SAA and cytokines in the context of HCV infection and highlight the dual role SAA could play in this disease. Nevertheless, more research is needed to establish whether the balance between those opposing activities can be tilted in favor of the host defense.