Lower Rates Of Naturally Occurring Resistance-Associated Substitutions (RASs) In Hepatitis C Virus (HCV)-Infected Chronic Kidney Disease (CKD) Patients Than In HCV-Infected Patients With Only Liver Disease

Ekta Gupta,1 Manish Chandra Choudhary,2 Nimisha Upadhyay,1 Gaurav Singh,1 Suman Lata Nayak,3 Manoj Kumar,4 Shiv Kumar Sarin4 1Department of Clinical Virology, ILBS, New Delhi, India; 2Department of Molecular and Cellular Medicine, ILBS, New Delhi, India; 3Department of Nephrology, ILBS, New Delhi, India; 4Department of Hepatology, ILBS, New Delhi, IndiaCorrespondence: Ekta GuptaDepartment of Clinical Virology, Institute of Liver & Biliary Sciences, New Delhi 110070, IndiaEmail ektagaurisha@gmail.comPurpose: Baseline viral load and existence of resistance-associated substitutions (RASs) are associated with direct-acting antiviral agent (DAA) treatment failure in patients with chronic hepatitis C virus (HCV) infection.Patients and methods: This study was done on HCV-infected patients with different clinical conditions, group 1 included HCV-infected patients with only liver disease (n= 24) and group 2 had HCV-infected patients with coexisting chronic kidney disease (CKD) (n =26). Baseline RAS in the viral genome, before treatment initiation, was examined in both the groups to understand the host disease status on their occurrence.Results: Predominant genotype (gt) differed in both the groups, in group 1 it was gt3 while it was gt1 in group 2. Overall, the occurrence of RASs at baseline was seen in 10 patients (20%); in group 1 it was seen in 8 (33.3%) as compared to only 2 (7.6%) in group 2; p < 0.001. RAS in both NS5a and NS5b regions of the virus was seen in group 1 while in group 2, RASs were seen only in the NS5a region of the virus at 30K position. In group 1, multiple RASs were also seen. The existence of RAS at baseline in both the groups did not affect the attainment of post-treatment cure for the virus in terms of sustained virological response (SVR).Conclusion: Host disease status influences the occurrence of baseline RAS in the virus.Keywords: Hepatitis C Virus infection, drug resistance, direct-acting antivirals