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The detected HCV genotypes and viral loads had both been extensively analysed. Many previous case reports had suggested that mean HCV RNA were higher in patients infected with genotype 1 were more likely to have higher viral loads than those infected with genotype 2 and 3. More selleck products efficient viral replication machinery of genotype 1 as compared to the others has been assumed to responsible for this [24]. However, the correlation between HCV genotypes and viral load remains controversial. In the present study the mean viral load in patients with genotype 3 was significantly higher than those with genotypes 1 and 2 but the correlation was not statistically significant (p-value>0.5). The results differ from a similar Pakistan based study where a high viral load was associated with genotypes 1a and 1b compared to other genotypes [25]. Our findings carry some important implication as timely detection and treatment are significant to achieve a high level of sustained virological response (SVR) [26]. Early time detection involves the identification of low HCV RNA level [5]. As determined by Von et al., and Dalgard et al., shorter therapy schedules for genotype 3 HCV infected patients with low baseline viral load could attain a SVR as compared to those with a high viral load [27,28]. Studies have shown that mixed HCV genotypes are more frequent in cases due to blood transfusion, especially in thalassaemic patients [26]. Franciscus had stated that mixed genotypes in a single patient may affect the antiviral therapy response and disease succession [29]. In the present study there were thalassaemic patients who had received unsafe blood in past. Fortunately, however no mixed genotype affected HCV cases were detected. Conclusion The present study results highlighted that genotype 3 is the predominant genotype in this geographical region followed by genotype1. However, no significant correlation was found between HCV genotypes and viral load in this study. The limitation of the study includes consideration of cases admitted only in a tertiary care hospital whereas a large number of chronic hepatitis patients are admitted in district and sub divisional hospitals. Multicentric study upon a larger population spanning over several years would have probably been helpful to further ascertain the correlation between viral genotypes and load. Our findings recommend that prior information about HCV genotype and basal RNA viral load should be an integral part of national planning strategies against HCV level at the therapeutic level. These results should help to individualize antiviral therapy, reduce side effects of antiviral therapy, economic burden and promote optimum response rates. Acknowledgments Authors acknowledge the Dr.