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Aim: Plasma Gas6 was tested as an alternative to Baveno VI criteria (liver stiffness 150 × 109/l) in an endoscopy-sparing strategy. Methods: A total of 160 patients with chronic hepatitis C and advanced fibrosis/cirrhosis underwent, on the same occasion, liver elastography, upper endoscopy, a platelet count and serum Gas6 measurement. Results: A total of 74/160 (46%) patients had esophageal varices, that were small (diameter

ABSTRACT: The elucidation of the mechanisms by which HCV infects hepatocytes and replicates has been paramount for identifying therapeutic targets and developing the highly efficacious antiviral drugs from which we benefit today. The earliest stage of HCV infection is viral entry, a process in which a complex interplay is thought to occur between host molecules (including glycosaminoglycans, low-density lipoprotein receptor, CD81, SR-B1, CLDN1, OCLN, EGF receptor, ephrin type A receptor 2 and transferrin receptor 1) and envelope viral glycoproteins E1 and E2. The wealth of experimental data produced in the field of HCV entry is summarized in a proposed mechanism, updated to include the most recently published data on the topic. Compounds with putative entry-blocking and/or entry-inhibiting activity in vitro and in vivo are also briefly reviewed.

Viral hepatitis has been treated empirically for more than 30 years with interferon (IFN)-based therapies, although in the early days of the IFN era, very little was known regarding the mechanisms of action through which IFN acts and the strategies that viruses deploy to escape the antiviral state induced by the activation of the IFN system. Over the years, we have learned how key effector molecules in this system are expressed and interact. On the verge of novel, IFN-free regimens for viral hepatitis, we can take advantage of this huge bulk of research data in order to gain better understanding of how resistance to IFN develops in our patients, to use IFN more effectively in conjunction with other drugs and to devise new treatments.