2 It is therefore evident that the presence of a risk factor is not a sufficient determinant of disease. Most researchers would deduce that fatal or drastic diseases based on genetic variation, in addition to those based on lethal mutations, are eliminated by natural selection on the long road of human evolution. Therefore, for the discovery of genetic variations showing a strong association with phenotype, the most effective research objective is directed FDA approved Drug Library research buy at patients treated with curative medicines that target that host factor. These drugs can be made with small molecular weight chemicals, human antibodies, or they can be obtained from natural products, modified to bring out the positive

effect against disease. Because human beings have not been under selective pressure of these medicines since recorded history, their contemporary pressure will reveal the fine results associated with clinical response to drug treatment. Based on this theory, we have started to discover genetic variations associated with response to chronic hepatitis C treatment using pegylated interferon and ribavirin. The SNPs obtained from whole genome analysis were reported by a number of research groups simultaneously in 2009

and many related studies have been uploaded to September 2011. The aim of Smad inhibitor this review is to summarize the relationship between genetic variation and hepatitis C infection. Since 2001, the standard of care for patients with chronic hepatitis C has been the combination of pegylated interferon (PEG-IFN) and ribavirin (RBV).3,4 This combination has produced sustained virologic response (SVR) rates of 50% to 60% in patients infected with hepatitis C virus (HCV) genotype 1 who adhere to the recommended therapeutic regimen, and 40% in intention-to-treat populations, as defined by an HCV RNA negative after 6 months of completing therapy (SVR). Transient viral response (TVR) is defined as re-appearance MCE公司 of HCV RNA in serum after treatment has been discontinued in a patient who had undetectable HCV RNA during the

therapy or on completion of the therapy (Fig. 1).3,4 In all, only about 65% of patients become HCV RNA-undetectable when treated with this regimen;3–5 the remaining one-third of all treated patients are classified as nonresponders (NR). Some of these patients have relatively mild liver disease but may have symptoms of HCV viremia, while others have advanced fibrosis and are at risk for developing liver complications, including decompensated cirrhosis and hepatocellular carcinoma, and the requirement for liver transplantation. Current therapies are limited by expense, ineffectiveness in a relatively high proportion of patients, numerous side effects, some of which are severe or which cause dose reduction and/or premature termination of treatment.