Host and Viral Factors and Changes in Liver Function Associated with Direct-Acting Antivirals Response in HCV Genotype-4 Patients

Abstract

Background and Aim: The response to DAAs therapy is attributed to a host of host and viral variables. Hepatitis C eradication is linked to considerable improvements in liver function and fibrosis. Several noninvasive methods for assessing hepatic fibrosis prior to HCV treatment have been developed and validated, all of which have a high level of reliability and clinical utility. However, their utility in assessing fibrosis progression after HCV eradication with DAAs is currently restricted. The aim of this study was to investigate into the potential significance of some host and viral characteristics in predicting direct-acting antiviral (DAAs) outcome and to assess changes in hepatic fibrosis and inflammation in chronic Hepatitis C genotype-4 patients treated with DAAs.
Subjects and Methods: A total of 150 CHC patients receivinga 12-week regimen of DAAs (SOF/DAV+RIB)were included in this study. Achieving sustained virologic response at 12weeks post-treatment(SVR12) was the main goal. Blood samples were withdrawn from allsubjects at baseline and 12 weeks after the end of treatment (EOT) for assessing viral load, liver transaminases levels, platelet count and other biochemical profiles in addition to calculating non-invasive biomarkers of liver fibrosis; fibrosis-4 index (FIB-4), Aspartate Aminotransferase-to-Platelet Ratio Index (APRI) score, AST/ALT ratio.Liver stiffness measurement (LSM) by FibroScan was performed prior treatment. Results: SVR to DAAs therapy was significantly correlated with HCV viral load and degree of liver fibrosis. SVR achieved by DAAs therapy was associated with significant improvement of non-invasive biomarkers of fibrosis (FIB-4, APRI score, and AAR) in addition to significant decrease in liver transaminases and elevation of platelet count from baseline compared to 12 weeks EOT (p ˂0.05).