Abstract
Hepatitis C virus (HCV) infects ~71 million people worldwide, and 399,000 people die annually due to HCV-related liver cirrhosis and hepatocellular carcinoma. The use of direct-acting antivirals results in a sustained virologic response in >95% of patients with chronic HCV infection. However, several issues remain to be solved to eradicate HCV. At the 26th International Symposium on Hepatitis C Virus and Related Viruses (HCV2019) held in Seoul, South Korea, October 5–8, 2019, virologists, immunologists, and clinical scientists discussed these remaining issues and how we can achieve the elimination of HCV.
Highlights
Hepatitis C virus (HCV) infects ~71 million people worldwide, and 399,000 people die annually due to HCV-related liver cirrhosis and hepatocellular carcinoma
At the 26th International Symposium on Hepatitis C Virus and Related Viruses (HCV2019) held in Seoul, South Korea, October 5–8, 2019, virologists, immunologists, and clinical scientists discussed these remaining issues and how we can achieve the elimination of HCV
71 million people worldwide are chronically infected with hepatitis C virus (HCV), and infected individuals are at an increased risk of liver cirrhosis and hepatocellular carcinoma (HCC) [1]
Summary
71 million people worldwide are chronically infected with hepatitis C virus (HCV), and infected individuals are at an increased risk of liver cirrhosis and hepatocellular carcinoma (HCC) [1]. The trial failed in terms of efficacy but was successful in terms of lessons for prophylactic HCV vaccine development In her plenary lecture, Young Nyun Park summarized the accumulation of pathological and molecular changes during hepatocarcinogenesis, from cirrhosis to low-grade dysplastic nodule, high-grade dysplastic nodule, and early HCC, and the final progression to HCC. Based on previous findings that HCV infection silences protein tyrosine phosphatase receptor delta (PTPRD) expression [4], Lupberger et al analyzed the transcriptome data from Ptprd knock-out mice and human liver They showed that PTPRD silencing by HCV might contribute to the development of HCV-associated metabolic disease, which is linked to deregulated STAT3 signaling and impaired peroxisomal function via suppression of peroxisome proliferator-activated receptor alpha (PPARA). This session expanded our understanding of the complex genomic and molecular networks that contribute to HCV-related liver disease pathogenesis
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