We recommend all patients should have the option of treatment, and have the pros and cons of opting for initiation of treatment

and of deferring treatment discussed with them. We suggest for patients with non-cirrhotic disease there is the option to defer treatment until newer therapies or a suitable trial become available. We recommend those deferring treatment are monitored by non-invasive tests at least annually and if they have confirmed progression of fibrosis are reconsidered for initiation of therapy. The response rates of genotypes 2 and 3 infection to pegylated interferon and ribavirin regimens are much higher than in genotype 1 infection in both monoinfected and coinfected individuals. In a recent meta-analysis, treatment response rates of genotype LDK378 mw 2 and 3 did not differ between HIV-infected and -uninfected populations [95]. Neither telaprevir nor boceprevir has substantial activity against genotypes 2 and 3, although second-generation protease inhibitors and other DAA classes as well as several interferon-sparing strategies have reported high rates of SVR in monoinfected populations [77,96–98]. Because of differential activity of the newer DAAs on GT2 and GT3 virus, there may be a requirement to separate recommendations in future guidelines [99–100].

Therefore the only available therapy for selleck kinase inhibitor genotype 2 and 3 hepatitis C in the context of HIV infection remains pegylated interferon and ribavirin. Ribavirin should be

prescribed as weight-based due to higher response rates when this method is employed. In individuals who are naïve to hepatitis C therapy, do not have cirrhosis (Metavir F4) and achieve an RVR, treatment duration should be 24 weeks, as longer courses of therapy have not translated into higher rates of SVR. Individuals not achieving an RVR but reaching an EVR should receive 48 weeks of therapy. All individuals receiving treatment after failing a previous interferon-based regimen should receive 48 weeks of therapy. Erythropoietin and granulocyte colony stimulating factors should be used as required and should be given in Unoprostone preference to interferon and ribavirin dose reduction. We suggest for patients with genotype 4 infection without cirrhosis, there is the option to defer treatment until newer therapies or a suitable clinical trial become available. We recommend if treatment is given now, this should be with pegylated interferon and ribavirin. The duration of therapy should be 48 weeks if RVR is achieved. If the RNA is still detectable at 12 weeks, consideration should be given to discontinuing treatment. For those with previous treatment failure, we recommend waiting for the availability of interferon-sparing regimens with active DAAs.