Hepatitis C virus reinfection after sustained virological response in HIV-infected patients with chronic hepatitis C

Juan A Pineda1, Rocio Núñez-Torres1, Francisco Téllez2

  • 1Unidad Clínica de Enfermedades Infecciosas y Microbiología, Hospital Universitario de Valme, Avda. de Bellavista s/n, 41014 Sevilla, Spain.

Insights

Hepatitis C virus (HCV) reinfection is low in HIV-coinfected patients who achieved sustained virological response. Low-risk behavior contributes to this, supporting HCV treatment in people who inject drugs.

Area of Science:

  • Infectious Diseases
  • Hepatology
  • Virology

Background:

  • Hepatitis C virus (HCV) infection is a significant concern in patients coinfected with HIV.
  • Achieving sustained virological response (SVR) through therapy is crucial for managing chronic hepatitis C.
  • Understanding reinfection rates is vital for long-term patient management and treatment strategies.

Purpose of the Study:

  • To determine the incidence of HCV reinfection in individuals coinfected with HIV who previously achieved SVR.
  • To identify factors associated with HCV reinfection in this population.
  • To inform treatment guidelines for HCV in HIV-coinfected patients, particularly people who inject drugs (PWID).

Main Methods:

  • Analysis of 84 HIV-infected patients with prior SVR after HCV treatment.
  • Regular HCV RNA monitoring over a median follow-up of 34 months.
  • Assessment of risk behaviors, including drug use and sexual practices, during follow-up.

Main Results:

  • Four out of 84 patients (4.76%) experienced HCV reinfection, with an incidence of 1.21 per 100 person-years.
  • Reinfected patients maintained risk factors for HCV transmission.
  • HCV genotype switching occurred in three cases, and one case suggested sexual transmission.

Conclusions:

  • The incidence of HCV reinfection after successful therapy in HIV-coinfected patients is low.
  • Low frequency of risk behaviors is the primary factor limiting reinfection rates.
  • The risk of reinfection should not deter the treatment of HCV with direct-acting antivirals, even in PWID.
Abstract

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