title: HCV-induced regulatory alterations of IL-1β, IL-6, TNF-α, and IFN-ϒ operative, leading liver en-route to non-alcoholic steatohepatitis.
abstract: Over the course of time, Hepatitis C has become a universal health menace. Its deleterious effects on human liver encompass a lot of physiological, genetic as well as epigenetic alterations. Fatty liver (Hepatic steatosis) is an inflammation having multifactorial ancestries; one of them is HCV (steatohepatitis). HCV boosts several cellular pathways involving up-regulation of a number of cytokines. Current study reviews the regulation of some selective key cytokines during HCV infection, to help generate an improved understanding of their role. These cytokines, IL-1β, IL-6, TNF-α, and IFN-ϒ, are inflammatory markers of the body. These particular markers along with others help hepatocytes against viral infestation. However, recently, their association has been found in degradation of liver on the trail heading to non-alcoholic steatohepatitis (NASH). Consequently, the disturbance in their equilibrium has been repeatedly reported during HCV infection. Quite a number of findings are affirming their up-regulation. Although these cell markers are stimulated by hepatocytes as their standard protection mechanism, but modern studies have testified the paradoxical nature of this defense line. Nevertheless, direct molecular or epigenetic research is needed to question the actual molecular progressions and directions commanding liver to steatosis, cirrhosis, or eventually HCC (Hepatocellular Carcinoma).
authors.affiliation: National Center of Excellence in Molecular Biology, University of the Punjab, Lahore, 54590, Pakistan.
authors.forename: Rabia
authors.initials: R
authors.lastname: Nawaz
authors.affiliation: National Center of Excellence in Molecular Biology, University of the Punjab, Lahore, 54590, Pakistan.
authors.forename: Sadia
authors.initials: S
authors.lastname: Zahid
authors.affiliation: Hazara University, Khyber Pakhtunkhawa, Dhodial, Pakistan.
authors.forename: Muhammad
authors.initials: M
authors.lastname: Idrees
authors.affiliation: National Center of Excellence in Molecular Biology, University of the Punjab, Lahore, 54590, Pakistan.
authors.forename: Shazia
authors.initials: S
authors.lastname: Rafique
authors.affiliation: National Center of Excellence in Molecular Biology, University of the Punjab, Lahore, 54590, Pakistan.
authors.forename: Muhammad
authors.initials: M
authors.lastname: Shahid
authors.affiliation: National Center of Excellence in Molecular Biology, University of the Punjab, Lahore, 54590, Pakistan.
authors.forename: Ammara
authors.initials: A
authors.lastname: Ahad
authors.affiliation: National Center of Excellence in Molecular Biology, University of the Punjab, Lahore, 54590, Pakistan.
authors.forename: Iram
authors.initials: I
authors.lastname: Amin
authors.affiliation: National Center of Excellence in Molecular Biology, University of the Punjab, Lahore, 54590, Pakistan.
authors.forename: Iqra
authors.initials: I
authors.lastname: Almas
authors.affiliation: National Center of Excellence in Molecular Biology, University of the Punjab, Lahore, 54590, Pakistan. samiaraza@live.com.
authors.forename: Samia
authors.initials: S
authors.lastname: Afzal
mesh_terms: D000818:Animals; D016207:Cytokines / Q000276:immunology*; D016174:Hepacivirus; D006526:Hepatitis C / Q000276:immunology*; D006801:Humans; D008099:Liver / Q000276:immunology*; D065626:Non-alcoholic Fatty Liver Disease / Q000276:immunology*
chemical_list: D016207:Cytokines
keywords: Hepatitis C virus (HCV); Interferon (IFN); Interleukins (IL); Non-alcoholic steatohepatitis (NASH); Tumor necrosis factor (TNF)