Inflammation and repair in viral hepatitis C

Manuela G. Neuman, Kevin Sha, Rustan Esguerra, Sam Zakhari, Robert E. Winkler, Nir Hilzenrat, Jonathan Wyse, Curtis L. Cooper, Devanshi Seth, Mark D. Gorrell, Paul S. Haber, Geoffrey W. McCaughan, Maria A. Leo, Charles S. Lieber, Mihai Voiculescu, Eugenia Buzatu, Camelia Ionescu, Jozsef Dudas, Bernhard Saile, Giuliano Ramadori

Research output: Contribution to journalReview articlepeer-review

29 Scopus citations


Hepatitis C viral infection (HCV) results in liver damage leading to inflammation and fibrosis of the liver and increasing rates of hepatic decompensation and hepatocellular carcinoma (HCC). However, the host's immune response and viral determinants of liver disease progression are poorly understood. This review will address the determinants of liver injury in chronic HCV infection and the risk factors leading to rapid disease progression. We aim to better understand the factors that distinguish a relatively benign course of HCV from one with progression to cirrhosis. We will accomplish this task by discussion of three topics: (1) the role of cytokines in the adaptive immune response against the HCV infection; (2) the progression of fibrosis; and (3) the risk factors of co-morbidity with alcohol and human immunodeficiency virus (HIV) in HCV-infected individuals. Despite recent improvements in treating HCV infection using pegylated interferon alpha (PEGIFN-α) and ribavirin, about half of individuals infected with some genotypes, for example genotypes 1 and 4, will not respond to treatment or cannot be treated because of contraindications. This review will also aim to describe the importance of IFN-α-based therapies in HCV infection, ways of monitoring them, and associated complications.

Original languageEnglish
Pages (from-to)1468-1487
Number of pages20
JournalDigestive Diseases and Sciences
Issue number6
StatePublished - Jun 2008


  • Chemokines
  • Cytokines
  • Fibrosis
  • HIV
  • Hepatitis C
  • Inflammation


Dive into the research topics of 'Inflammation and repair in viral hepatitis C'. Together they form a unique fingerprint.

Cite this