Liver fibrosis progression in human immunodeficiency virus and hepatitis C virus coinfected patients. The Multivirc

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Establishment of the Dual Humanized TK-NOG Mouse Model for HIV-associated Liver Pathogenesis
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Published on: September 11, 2019

Y Benhamou1, M Bochet, V Di Martino

  • 1Service d'Hépato-Gastroentérologie, Groupe Hospitalier Pitié Salpêtrière and UPRES-A 8067, Paris, France. ybenhamou@teaser.fr

Hepatology (Baltimore, Md.)
|September 25, 1999
PubMed

Insights

Human immunodeficiency virus (HIV) and hepatitis C virus (HCV) coinfection accelerates liver fibrosis progression. Factors like low CD4 count and alcohol consumption significantly increase fibrosis rates in coinfected patients.

Area of Science:

  • Hepatology
  • Virology
  • Immunology

Background:

  • The natural history of hepatitis C virus (HCV) in human immunodeficiency virus (HIV)-infected individuals, particularly concerning liver fibrosis progression, remains understudied.
  • Understanding fibrosis progression is crucial for managing coinfections and preventing liver disease complications.

Purpose of the Study:

  • To assess and compare the fibrosis progression rate in patients coinfected with HIV and HCV versus those with HCV infection alone.
  • To identify factors associated with accelerated liver fibrosis in HIV-HCV coinfected patients.

Main Methods:

  • A cohort study comparing 122 HIV-HCV coinfected patients with 122 HCV-monoinfected controls, matched for key demographic and exposure variables.
  • Fibrosis progression rate calculated using the METAVIR scoring system and duration of HCV infection.
  • Statistical analysis to identify factors associated with increased fibrosis progression rate.

Main Results:

  • HIV-HCV coinfected patients exhibited higher rates of extensive liver fibrosis and moderate/severe liver activity compared to HCV-monoinfected patients.
  • The median fibrosis progression rate was significantly higher in coinfected patients (0.153 units/year) than in controls (0.106 units/year).
  • HIV seropositivity, alcohol consumption (>50 g/d), younger age at HCV infection (<25 years), and severe immunosuppression (CD4 count ≤200 cells/μL) were independently associated with increased fibrosis progression.

Conclusions:

  • HIV coinfection significantly accelerates the progression of liver fibrosis in patients with hepatitis C virus.
  • In HIV-HCV coinfected individuals, factors such as low CD4 count, high alcohol consumption, and early age of HCV infection are critical determinants of rapid fibrosis progression.
  • These findings underscore the importance of managing HIV, alcohol intake, and timely HCV treatment in coinfected patients to mitigate liver disease progression.

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