[ANRS HC 02 RIBAVIC: histo-pathological impact]

Area of Science:

• Hepatology
• Virology
• Immunology

Background:

• Hepatitis C virus (HCV) therapy can lead to sustained virologic response (SVR), improving liver health.
• Fibrosis and cirrhosis reduction are observed post-SVR, but data in HIV-HCV co-infected patients are limited.

Purpose of the Study:

• To evaluate the impact of antiviral therapy on liver fibrosis in HIV-HCV co-infected patients.
• To identify factors associated with fibrosis progression and liver events in this population.

Main Methods:

• Analysis of paired liver biopsies (Metavir and Ishak scores) from 205 HIV-HCV co-infected patients in the RIBAVIC ANRS HC02 trial.
• Prospective follow-up of 383 co-infected patients in the RIBAVIC cohort for a median of 60 months.

Main Results:

• SVR was associated with reduced necro-inflammation and fibrosis stabilization, while non-response led to stabilization.
• No fibrosis reversal was observed even with SVR; didanosine and non-response correlated with fibrosis deterioration.
• In the RIBAVIC cohort, liver events occurred in 5% of patients, primarily non-responders with advanced fibrosis (F3).
• Multivariate analysis identified virologic response, fibrosis score < F3, and baseline CD4 count > 350/mL as survival factors.

Conclusions:

• Antiviral therapy improves liver necro-inflammation in HIV-HCV co-infected patients, but fibrosis reversal is not achieved.
• Virologic non-response and potential antiretroviral toxicity (e.g., didanosine) contribute to fibrosis worsening.
• Early intervention to maximize SVR rates is essential for preventing severe liver complications in co-infected patients.