Background: Over 80 million people are infected globally with chronic HCV. It promotes inflammation and, hence. hepato-carcinogenesis. As a result, resolving HCV infection should result in decreased incidence of hepatocellular carcinoma. Oral DAAs introduction has changed overall prognosis of HCV. SVR has been linked to improved liver function as well as a reduction in clinical consequences and all-cause mortality. Monocytes and macrophages generate CD163, a hemoglobin scavenger receptor. In a variety of hepatic and viral disorders, soluble CD163 is a well-established marker of portal hypertension and disease severity. In addition, in chronic HCV infection there have been strong connections between macrophage activation, histological inflammation and fibrosis. Our goal is to assess the role of soluble CD163 as a surrogate marker for detection of fibrosis regression in HCV patients treated with direct antiviral agents.Results: Forty chronic HCV patients and ten healthy subjects were included in this study. Serum sCD163 was tested before and 12 weeks after treatment by DAAs. Mean values of sCD163 were statistically significantly higher in chronic HCV case group in comparison to control group, and they showed statistically significant decline after achievement of SVR12 weeks with p value of <0.001. On calculating different fibrosis scoring scores (APRI and FIB-4) differences between pretreatment and SVR12 results showed no statistical significance. While on applying fibroscan a significant down-staging was detected in fibrosis scores 12 weeks after achieving SVR. our study demonstrated that the best cut-off values of baseline sCD163 in detection of liver cirrhosis was >6.2 ng/ml with 87.50% sensitivity, 95.83% specificity, with overall accuracy of 97.2%. Conclusion: sCD163 serum level declines with successful DAA therapy and is associated with regression in staging of fibrosis supporting its promising role in monitoring treatment response rather than other methods of fibrosis measurement.