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Hepatitis C Virus (HCV) Inhibits Normal Immune Response by Triggering Suppressor of Cytokine Signaling (SOCS) Regulator Molecule
Scientists from Trinity College Dublin have discovered how the highly infectious and sometimes deadly hepatitis C virus (HCV) "ghosts" our immune system and remains undiagnosed in many people. The rsearchers reported their findings on June 5, 2019 in The FASEB Journal. The article is titled “The Hepatitis C Virus (HCV) Protein, P7, Suppresses Inflammatory Responses to Tumor Necrosis Factor (TNF)-α Via Signal Transducer and Activator of Transcription (STAT)3 and Extracellular Signal-Regulated Kinase (ERK)–Mediated Induction of Suppressor of Cytokine Signaling (SOCS)3.” HCV's main route of transmission is via infected blood, but over the past 40 years, the virus has accidentally been given to many patients across the world via infected blood products. The virus replicates particularly well in the liver, and the damage it causes makes it a leading cause of liver disease worldwide. Even though HCV can be deadly, initial infection is rarely accompanied by any obvious clinical symptoms for reasons that have, until now, remained unknown. As a result, it often goes undiagnosed for the first 6-12 months following infection. If left untreated, HCV spreads throughout the liver, stimulating a low-level inflammatory response. Over several months, these mild responses, accompanied by subsequent liver repair, result in fibrotic scarring of the liver. The liver's main job is to filter out toxins, but during HCV infection the build-up of fibrotic, non-functioning liver tissue, results in reduced liver function. Without a fully functioning liver, one major side-effect is the build-up of toxins, often manifest as "jaundice.” If patients do not realize they are infected with HCV, their first noticeable symptoms are the side-effects of liver fibrosis (such as jaundice).