Ifnl3, also known as IL28B, is a gene that plays a crucial role in the body's immune response, particularly in antiviral defense. It belongs to the interferon lambda family, and its encoded protein can activate an antiviral response by binding to a specific receptor complex, triggering signaling pathways involved in innate immunity [4].

Polymorphisms near Ifnl3, such as rs12979860 and rs8099917, have been associated with the response to interferon-based therapy in chronic hepatitis B (CHB) patients, especially in the HBeAg-positive group [1]. In COVID-19 patients, the rs8099917 polymorphism of Ifnl3 is associated with an increased likelihood of a lethal outcome [2]. Additionally, the rs12979860 polymorphism near Ifnl3 is associated with pulmonary fibrosis in systemic sclerosis patients, and IFN-λ3 serum levels are higher in those with pulmonary fibrosis [3]. In hepatitis C virus (HCV) infections, Ifnl3 SNPs are strong predictors of sustained virologic response to pegylated interferon and ribavirin therapy in genotype 1, 2, and 3 infections [6]. Intrahepatic Ifnl3 expression is lower in chronic HCV carriers compared to healthy controls and is higher in the early stages of liver fibrosis [5].

In conclusion, Ifnl3 is essential for the body's antiviral immune response. Genetic studies, especially those focusing on polymorphisms, have revealed its significant associations with various diseases, including viral hepatitis, COVID-19, and pulmonary fibrosis. These findings highlight the importance of Ifnl3 in disease pathogenesis and its potential as a biomarker for treatment response and disease prognosis.