Coinfected patients may require longer HCV treatment, irrespective of genotype

Simon Collins, HIV I-Base

Recent clinical implications for management of patients with Hepatitis C and HIV coinfection include an opportunity to recognise non-responders at 12 weeks, and therefore reduce exposure to unnecessary treatment, and at the other extreme, that a longer period of treatment may be necessary for others.

Vincent Soriano and colleagues presented further important data on response rates for 89 coinfected Spanish patients who completed a course of PEG interferon plus ribavirin at standard doses.

Although 58% patients achieved >2log reductions in HCV viral load by week 12, only half of these patients achieved a sustained virologic response (SVR). None of the patients who had less than a two log drop at week 12 achieved an SVR.

Relapses occurred in 19 – almost one third – of the 58 patients who had negative HCV RCR at the end of the treatment period, and there were no significant differences in response between patients with genotype 2/3 and genotype 1/4.

The authors commented that the 100% negative predictive value for non-responders was previously reported in HCV monoinfected patients and could be used to discontinue a difficult to tolerate treatment. The higher relapse rate compared to monoinfected patients, particularly those with genotype 2/3 who rarely rebound, prompted the suggestion to extend treatment from six to 12 months in coinfected patients with genotype 2/3 and from 12 to 18 months fro those with genotype 1/4.


Soriano V, Perez-Olmeda M, Camino N et al. Clinical implications of the slower clearance of HCV-RNA under Interferon (IFN) plus ribavirin (RBV) in patients coinfected with HIV and Hepatitis C virus (HCV). 43 ICAAC. Abstract H-1718.


This study highlights, as have studies with singular HCV infection, the reliability of early virological response (EVR) in predicting end of therapy responses (ETR) and sustained responses (SR). EVR is defined as an undetectable HCV-RNA or >2 log drop n HCV-RNA levels 12 weeks after starting therapy.

It is of note that despite EVR only half of these patients went on to achieve SRs and that 33% of patients with an ETR had a relapse on stopping therapy. The length of therapy was 24 weeks for genotypes 2/3 patients and 48 weeks for genotype 1 patients. The high relapse rate may be as a result of viral sanctuary sites or emergence of ‘escape’ quasispecies. If the former is true then extending treatment beyond the standard 24 or 48 weeks may be helpful in reducing relapse rates, as suggested by the authors.

The answer to this question, in part, may come from the currently ongoing Apricot study, which is due to report initial results early next year. In this study all patients irrespective of genotypes have received 48 weeks of therapy.

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