Molecular And Phylogenetic Characterization of HCV Core Gene Among Hemodialysis Patients in Iraq
DOI:
https://doi.org/10.67440/ahj.vi.2050Abstract
Hepatitis C virus (HCV) is a serious public health concern worldwide due to a high incidence of chronic infection and long-term liver-related sequelae. Although curative direct-acting antiviral medication is available, recent estimates suggest that tens of millions of people continue to live with chronic HCV infection globally. This is clinically essential as persistent HCV infection leads to progressive liver injury and is a leading cause of chronic hepatitis, cirrhosis, end-stage liver disease and hepatocellular carcinoma[1,2,3]. At the molecular scale, HCV is an enveloped, positive-sense single-stranded RNA virus of the family Flaviviridae with a genome of roughly 9.4–9.6 kb with a single large open reading frame encoding a viral polyprotein[4]. The clinical and epidemiological relevance of HCV is further compounded in patients on hemodialysis, a population that continues to be overrepresented in blood-borne infections[5,6]. Hemodialysis (HD) is the main renal replacement therapy to increase the survival and quality of life of people with CKD. However, the HD approach is associated with impaired cellular immune response in the patients and hence predisposes them to a variety of blood-borne viral infections. The risk of transmission of hepatitis B virus (HBV), hepatitis C virus (HCV) and human immunodeficiency virus (HIV) in the HD population is complex. The important risk factors are percutaneous exposure, past blood transfusions, advanced age, longer duration of dialysis therapy and probable contamination of HD machines and associated apparatus[7]. HCV is considered both a cause and a consequence of chronic kidney disease (CKD). Besides HCV-linked glomerulonephritis, the virus causes CKD through multiple mechanisms, leading to incident CKD and progression to end-stage renal disease requiring hemodialysis or transplantation.

