A REVIEW ARTICLE ON IFN-Y AND FOXP-3 IN HEPATITIS C VIRUS INFECTION

Hepatitis C virus (HCV), which belongs to the Hepacivirusgenus in the Flaviviridae family and contains a single-stranded positive-sense RNA genome, has emerged as a common cause of liver-related disorders worldwide. The genome of HCV is approximately 9,600 bases long and contains a large open reading frame (ORF). This ORF is linked to 5 and 3 untranslated regions (UTRs). The immune system, both the innate and adaptive responses, plays a vital role in HCV infection. These immune responses towards HCV infection include different cytokines and immune cells. During HCV infection, Interferon-gamma (IFN Y) and Fork-head box protein P3 (FOXP3) genes play a significant role in managing the immune responses. IFN Y, being a type-II cytokine, promotes the control of viral replication and clearance of infected hepatocytes during HCV infection. Studies have reported that higher expression of IFN Y is linked with a better prognosis, and there is more likelihood of viral clearance. On the other side, FOXP3 is a transcription factor that is essential for the development and functioning of regulatory T cells (Tregs), which are important for maintaining immune tolerance and preventing autoimmunity. FOXP3 Tregs play a dual role in HCV infection. They downregulate excessive immune responses and prevent liver damage by controlling effector T cell activity. The efficiency of antiviral response is limited by the immunosuppressive function of FOXP3. In conclusion, IFN-Y and FOXP3 have a vital role during HCV infection, focusing on the dynamic and complex nature of the host virus interaction. The IFN-Y is important for the antiviral immune response in HCV infection. However, the activity of IFN-Ymust be controlled to prevent immunopathology. Similarly, FOXP3 Tregs play a protective role in reducing liver inflammation as well as damage to liver cells. FOXP3 can also facilitate the virus to persist in the liver cells, which can lead to a chronic HCV infection.