"IFN I understand, but ribavirin?"
the moa of both in and rib are poorly understood. ribavirin is less potent in reducing VL, but suppresses relapse putatively through some immune-mediated phenomena
"Have you seen any data to support this"
no - because no one has run a trial aimed at looking at SVR without IN (unlike ribavirin - which to date have met with failure, the most prominent of which was idix's nm-283. at the time the CEO said ribavirin seems to work some "magic" to suppress relapse, and a roundtable with thought leaders shortly therafter that i listened to said betting against ribavirin was a losing proposition)
softer evidence comes from direct antiviral monotherapy trials, where rapid resistance was seen. the notion that combination therapy with direct antivirals, like HIV therapy, will dramatically suppress resistance is nto far-fetched except unlike HIV the goal is a cure. while HCV doesn't integrate into the genome like HIV, most feel some immune boosting is necessary to achieve cure (or more aptly maintain durable response). why? data on pts who achieved SVR who are then given immunosuppressants (say s/p liver transplantation) show rebound of virus - so there seems to be some reservoir of virus outside the liver, and the immune system appears critical to maintaining sustained viral response - so you can see my skepticism in any regimen that does not include some immune modulator.
I think a major reason why companies continue to try and replace ribavirin and not IN is not jsut due to tooxicity of the former, but because IN alone can (albeit with less success) achieve cure, wherease ribavirin alone has no chance at cure and no proof of principle exists that ribavirin without interferon can achieve the necessary immune modulation to maintain viral suppression once antiviral therapy is discontinued
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