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Vertex Pharmaceuticals Incorporated Message Board

  • thirdmeinvestor thirdmeinvestor Sep 23, 2009 7:58 PM Flag

    Human genetic variants that clear HCV

    If you listened to the Morgan Stanley conf. session given a week ago, you may recall the following question by the MS analyst: where does TVR stand in the wake of the finding that a patient group (~20%) who have a certain genetic makeup can clear HCV with SOC alone with an 80% SVR rate. I found 4 Nature and Nature Genetics papers' abstracts, all of which agree on the conclusion. Kurt Graves immediately gave a perfect answer. If the patients with this type of genes were treated with TVR and SOC they can be cured by 24 wk treatment instead of 48 wk one. Besides, the genotyping used to screen for such a polymorphism costs thousands of dollars. Below I paste an abstract of one Nature paper. Note that McHutchison is among the authors.

    Genetic variation in IL28B predicts hepatitis C treatment-induced viral clearance.Ge D, Fellay J, Thompson AJ, Simon JS, Shianna KV, Urban TJ, Heinzen EL, Qiu P, Bertelsen AH, Muir AJ, Sulkowski M, McHutchison JG, Goldstein DB.
    Institute for Genome Sciences & Policy, Center for Human Genome Variation, Duke University, Durham, North Carolina 27708, USA.

    Chronic infection with hepatitis C virus (HCV) affects 170 million people worldwide and is the leading cause of cirrhosis in North America. Although the recommended treatment for chronic infection involves a 48-week course of peginterferon-alpha-2b (PegIFN-alpha-2b) or -alpha-2a (PegIFN-alpha-2a) combined with ribavirin (RBV), it is well known that many patients will not be cured by treatment, and that patients of European ancestry have a significantly higher probability of being cured than patients of African ancestry. In addition to limited efficacy, treatment is often poorly tolerated because of side effects that prevent some patients from completing therapy. For these reasons, identification of the determinants of response to treatment is a high priority. Here we report that a genetic polymorphism near the IL28B gene, encoding interferon-lambda-3 (IFN-lambda-3), is associated with an approximately twofold change in response to treatment, both among patients of European ancestry (P = 1.06 x 10(-25)) and African-Americans (P = 2.06 x 10(-3)). Because the genotype leading to better response is in substantially greater frequency in European than African populations, this genetic polymorphism also explains approximately half of the difference in response rates between African-Americans and patients of European ancestry.

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