The correlation between pretreatment cytokine expression patterns in peripheral blood mononuclear cells with chronic hepatitis c outcome

Abstract

BackgroudCytokine response against hepatitis C virus (HCV) is likely to determine the natural course of infection as well as the outcome of antiviral treatment. However, the role of particular cytokines remains unclear. The current study analyzed activation of cytokine response in chronic hepatitis C patients undergoing standard antiviral treatment.MethodsTwenty-two patients were treated with pegylated interferon and ribavirin. Twenty-six different cytokine transcripts were measured quantitatively in peripheral blood mononuclear cells (PBMC) before and after therapy and correlated with therapy outcome as well as with clinical and liver histological data.ResultsWe found that patients who achieved sustained virological response (SVR) showed higher pretreatment cytokine response when compared to subjects in whom therapy was unsuccessful. The differentially expressed factors included IL-8, IL-16, TNF-α, GM-CSF, MCP-2, TGF-β, and IP-10. Serum ALT activity and/or histological grading also positively correlated with the expression of IL-1α, IL-4, IL-6, IL-10, IL-12, IL-15, GM-CSF, M-CSF, MCP-2 and TGF-β.ConclusionPretreatment activation of the immune system, as reflected by cytokines transcripts upregulation, positively correlates with treatment outcome and closely reflects liver inflammatory activity.

Influence of hepatitis C virus eradication with direct‐acting antivirals on the gut microbiota in patients with cirrhosis

“…Our study also confirms that the production of inflammatory cytokines and chemokines is enhanced in patients with chronic HCV infection and is downregulated by viral eradication . Indeed, antiviral therapy significantly improved IL1‐ra, IL2, IL5, FGF‐basic, GM‐CSF, IFN‐gamma, CCL2, CCL3, CCL4, CCL11, CXCL10, PDGF‐BB, and TNF‐alpha plasma levels.…”

“…Indeed, this result may be affected by the relatively short follow-up period, as the evaluation of these parameters was performed 1 year after the end of the DAA treatment, and also by the fact that only patients with well-compen- Our study also confirms that the production of inflammatory cytokines and chemokines is enhanced in patients with chronic HCV infection and is downregulated by viral eradication. [28][29][30][31][32][33][34][35][36][37] Indeed, antiviral therapy significantly improved IL1-ra, IL2, IL5, FGF-basic, , faecal calprotectin) before and 1 y after the end of direct-acting antiviral (DAA) treatment. IL: interleukin; ra:receptor agonist; FGF: fibroblast growth factor; G-CSF: granulocyte colony-stimulating factor; GM-CSF: granulocytemacrophage colony-stimulating factor; IFN: interferon; CCL: C-C motif chemokine ligand; CXCL: C-X-C motif chemokine ligand; PDGF: plateletderived growth factor; TNF: tumour necrosis factor GM-CSF, IFN-gamma, CCL2, CCL3, CCL4, CCL11, CXCL10, PDGF-BB, and TNF-alpha plasma levels.…”

IFN‐free therapy is associated with restoration of type I IFN response in HIV‐1 patients with acute HCV infection who achieve SVR

“…In addition, there is little known about the host‐virus interactions in the setting of DAAs and how the immune system will respond to the inhibition of replication without concomitant exogenous interferon administration. It is well established that chronic HCV is associated with changes in innate immune responses characterized by the upregulation of interferon‐stimulated genes (ISGs) and elevations in several relevant IFN‐sensitive chemokines and cytokines . The degree of host immune dysregulation has been associated with treatment outcomes with IFN‐based therapy, and HCV eradication with IFN‐based regimens has been shown to restore ISG and type I IFN responses .…”

HBV/HCV dual infection impacts viral load, antibody response, and cytokine expression differently from HBV or HCV single infection

“…Pro-inflammatory cytokines such as IL-6, IL-8, and TNF-α are involved in HBV- or HCV-induced liver inflammation and treatment outcomes2740414243. The expression levels of these cytokines in HBV/HCV dual infection are unclear.…”