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Published on: January 7, 2019
Sustained virological response to peginterferon therapy in patients infected with HCV (genotypes 2 and 3), with or
Insights
HIV/HCV coinfection does not significantly impact sustained virological response (SVR) rates compared to HCV monoinfection. Treatment outcomes for hepatitis C virus (HCV) are similar regardless of HIV status.
Area of Science:
- Hepatology
- Infectious Diseases
- Virology
Background:
- HIV infection accelerates liver disease progression in patients with Hepatitis C Virus (HCV).
- Prior studies indicated lower sustained virological response (SVR) rates in HIV/HCV coinfection versus HCV monoinfection.
Purpose of the Study:
- To compare SVR rates between HCV monoinfected and HIV/HCV coinfected patients.
- To identify predictors of SVR in these populations.
Main Methods:
- Retrospective analysis of clinical, biochemical, and virological data.
- Inclusion of patients with HCV genotypes 2 and 3 treated between 2004-2012.
- Intention-to-treat (ITT) and per-protocol (PP) analyses, with logistic regression for predictor assessment.
Main Results:
- No statistically significant difference in SVR rates between HCV monoinfected and HIV/HCV coinfected groups in either ITT (78.2% vs 68.4%) or PP (83.6% vs 84.9%) analyses.
- Baseline differences observed: HCV monoinfected patients had higher prevalence of genotype 2, higher viral load, shorter treatment duration, and less cirrhosis.
- HIV/HCV coinfected patients showed a higher prevalence of cirrhosis (31.6% vs 6%).
Conclusions:
- Higher baseline viral loads and treatment interruptions were associated with poor anti-HCV treatment outcomes.
- HIV infection itself was not found to be a significant factor affecting the probability of achieving SVR.
Background:
HIV infection leads to a faster progression of liver disease in subjects infected with HCV, as compared with HCV mono-infected patients. Previous reports suggest that sustained virological response (SVR) rates are lower in HIV/HCV coinfection than in HCV monoinfection. We aimed to compare SVR rates of these two populations.
Methods:
We retrospectively analyzed clinical, biochemical and virological data of HCV and HIV/HCV infected patients with HCV genotypes 2 and 3 who started anti-HCV treatment between March 2004 and November 2012, at a single large center. Intention-to-treat (ITT) and per-protocol (PP) analysis were performed. Univariate and multivariate logistic regression analyses were performed to assess predictors of SVR.
Results:
461 patients were analyzed: 307 (66.6%) males, 76 (16.5%) infected with HIV. Several differences at baseline between HCV monoinfected and HIV/HCV coinfected patients were observed. HCV monoinfected group was characterized by higher prevalence of genotype 2 (53% vs 5.3%), higher baseline HCV viral load (50% vs 35%), shorter mean duration of treatment (19 vs 41 weeks), more frequent use of peginterferon alfa-2a (84.5% vs 69.7%), lower prevalence of cirrhosis (6% vs 31.6%). Globally, SVR was achieved by 353 (76.6%) patients and 321 (83.8%) in the PP analysis. No statistically relevant differences were found in SVR rates between the two groups, either in ITT [78.2% (n = 301/385) vs 68.4% (n = 52/76), p =0.066, respectively] than in PP analysis [83.6% (n = 276/330) vs 84.9% (n = 45/53), p = 0.8].
Conclusions:
Higher baseline viral loads and interruption of peginterferon and/or ribavirin were associated with a poor outcome of anti-HCV treatment while HIV infection was not related to major or minor probability to achieve SVR.
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