HCV usually induces a robust immune response but it has developed mechanisms to escape immune defense and establish persistent infection. Recent reports indicate that 12.5 million people are infected in India and the number is steadily increasing day by day. As per current guidelines for clinical practice, HCV Anemarsaponin-BIII genotype and HCV RNA levels at baseline are considered to be an important marker before starting the antiviral interferon therapy but studies show that the treatment progression is often marred by side effects which ultimately force the patients to discontinue the therapy. Ge et al., found that Hexamethonium Bromide rs12979860 single nucleotide polymorphism, located 3 kb upstream of the IL28B gene was the strongest host predictor for treatment response in HCV patients infected with genotype 1 strain. Tanaka et al., found rs8099917, another IL28B polymorphism which is located around 8 kb upstream of the IL28B gene, to be the strongest genetic determinant of SVR in HCV genotype 1 infected patients. Initially, most of the studies have concentrated on the HCV genotype 1 as this genotype is more common in western countries. However, the impact of these polymorphisms within genotype 3 HCV infected individuals remains understudied. Reports have also indicated that ethnic differences in the IL28B gene polymorphisms may explain at least in part, the different outcome rates of HCV infection in different population groups. Differences in treatment outcome with respect to antiviral treatment have led the researchers in the present study to ascertain the frequency of IL28B host genotype within different population groups in eastern and north eastern India. The Indian population is ethnically heterogeneous; therefore, genetic variability is expected. Not much data are available about the frequency of host genotype rs12979860 or rs8099917 in India, a study conducted by Sivaprasad et al, amongst south Indian population demonstrated that the proportion of CC allele was higher than the proportion of CT, TT at rs12979860 alleles in the south Indian population, but the study concentrated only on the proportion of the host alleles amongst the healthy individuals. Our study on the other hand analyzed both the healthy individuals as well as HCV infected individuals, to get a clear picture of the genetic disposition of the host genotypes. In this study, analysis of healthy individuals showed that our data is in concordance with the data obtained by Sivaprasad et albut the percentage of favourable CC allele at rs12979860 locus was higher at 73% in contrast to 59.09%. Additionally, our study analyzed the host genetic disposition at both rs12979860 and rs8099917 amongst healthy individuals which was not done elsewhere. The association between IL28B polymorphism and the progression of liver fibrosis is still controversial, as the possible underlying mechanisms are still unknown to us. Within our study population, viral genotype 3 was found to be most widely circulated strain; HCV genotype 3 is reportedly associated with steatosis and rapid progression to HCC. Due to its association with steatosis, we have studied the proportion of IL28B genotypes in HCV infected patients in different stages of advanced liver diseases. We observed that the percentage of unfavourable CT and TG allele were more in these patients as compared to favourable CC and TT allele at rs12979860 and rs8099917 respectively. Several reports indicate strong association between IL28B polymorphism and SVR; the mechanisms are still not properly understood.