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      Hepatitis C Virus and Hepatocellular Carcinoma: Pathogenetic Mechanisms and Impact of Direct-Acting Antivirals

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          Abstract

          Introduction:

          Globally, between 64 and 103 million people are chronically infected with Hepatitis C virus (HCV), with more than 4.6 million people in the United States and is associated with more than 15.000 deaths annually. Chronic infection can result in cirrhosis and hepatocellular carcinoma.

          Explanation:

          Epidemiological studies have indicated that persistent infection with hepatitis C virus (HCV) is a major risk for the development of hepatocellular carcinoma (HCC), mainly through chronic inflammation, cell deaths, and proliferation. Despite the new direct-acting antiviral drugs (DAA’s) being able to clear the HCV, HCC recurrence rate in these patients is still observed.

          Conclusion:

          In this review we highlighted some aspects that could be involved in the onset of HCV-induced HCC such as immune system, viral factors and host genetics factors.

          Moreover, we focused on some of the last reports about the effects of DAA’s on the HCV clearance and their potential implications in HCC recurrence.

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          HCC and angiogenesis: possible targets and future directions.

          Andrew Zhu, Dan G Duda, Dushyant V Sahani … (2011)
          Hepatocellular carcinoma (HCC), the most common primary liver tumor, is notoriously resistant to systemic therapies, and often recurs even after aggressive local therapies. HCCs rely on the formation of new blood vessels for growth, and VEGF is critical in this process. A hallmark of new vessel formation in tumors is their structural and functional abnormality. This leads to an abnormal tumor microenvironment characterized by low oxygen tension. The liver is perfused by both arterial and venous blood and the resulting abnormal microenvironment selects for more-aggressive malignancies. Anti-VEGF therapy with sorafenib was the first systemic therapy to demonstrate improved survival in patients with advanced-stage HCC. This important development in the treatment of HCC raises hope as well as critical questions on the future development of targeted agents including other antiangiogenic agents, which hold promise to further increase survival in this aggressive disease.
          Article 0 comments Cited 201 times – based on 0 reviews     Review now
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            Impact of pegylated interferon alfa-2b and ribavirin on liver fibrosis in patients with chronic hepatitis C.

            Thierry Poynard, John G McHutchison, Michael Peter Manns … (2002)
            Liver fibrosis is an important prognostic factor in patients with hepatitis C. The effect of pegylated (PEG) interferon alone or its combination with ribavirin on fibrosis has not been established. We pooled individual data from 3010 naive patients with pretreatment and posttreatment biopsies from 4 randomized trials. Ten different regimens combining standard interferon, PEG interferon, and ribavirin were compared. The impact of each regimen was estimated by the percentage of patients with at least 1 grade improvement in the necrosis and inflammation (METAVIR score), the percentage of patients with at least 1 stage worsening in fibrosis METAVIR score, and by the fibrosis progression rate per year. Necrosis and inflammation improvement ranged from 39% (interferon 24 weeks) to 73% (optimized PEG 1.5 and ribavirin; P < 0.001). Fibrosis worsening ranges from 23% (interferon 24 weeks) to 8% (optimized PEG 1.5 and ribavirin; P < 0.001). All regimens significantly reduced the fibrosis progression rates in comparison to rates before treatment. The reversal of cirrhosis was observed in 75 patients (49%) of 153 patients with baseline cirrhosis. Six factors were independently associated with the absence of significant fibrosis after treatment: baseline fibrosis stage (odds ratio [OR] = 0.12; P < 0.0001), sustained viral response (OR = 0.36; P < 0.0001), age < 40 years (OR = 0.51; P < 0.001), body mass index < 27 kg/m(2) (OR = 0.65; P < 0.001), no or minimal baseline activity (OR = 0.70; P = 0.02), and viral load < 3.5 millions copies per milliliter (OR = 0.79; P = 0.03). PEG-interferon and ribavirin combination significantly reduces the rate of fibrosis progression in patients with hepatitis C.
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              Interferon-lambda: a new addition to an old family.

              Raymond P. Donnelly, Sergei V. Kotenko (2010)
              The discovery and initial description of the interferon-lambda (IFN-lambda) family in early 2003 opened an exciting new chapter in the field of IFN research. There are 3 IFN-lambda genes that encode 3 distinct but highly related proteins denoted IFN-lambda1, -lambda2, and -lambda3. These proteins are also known as interleukin-29 (IL-29), IL-28A, and IL-28B, respectively. Collectively, these 3 cytokines comprise the type III subset of IFNs. They are distinct from both type I and type II IFNs for a number of reasons, including the fact that they signal through a heterodimeric receptor complex that is different from the receptors used by type I or type II IFNs. Although type I IFNs (IFN-alpha/beta) and type III IFNs (IFN-lambda) signal via distinct receptor complexes, they activate the same intracellular signaling pathway and many of the same biological activities, including antiviral activity, in a wide variety of target cells. Consistent with their antiviral activity, expression of the IFN-lambda genes and their corresponding proteins is inducible by infection with many types of viruses. Therefore, expression of the type III IFNs (IFN-lambdas) and their primary biological activity are very similar to the type I IFNs. However, unlike IFN-alpha receptors which are broadly expressed on most cell types, including leukocytes, IFN-lambda receptors are largely restricted to cells of epithelial origin. The potential clinical importance of IFN-lambda as a novel antiviral therapeutic agent is already apparent. In addition, preclinical studies by several groups indicate that IFN-lambda may also be useful as a potential therapeutic agent for other clinical indications, including certain types of cancer.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Open Virol J
                Journal ID (iso-abbrev): Open Virol J
                Journal ID (publisher-id): TOVJ
                Title: The Open Virology Journal
                Publisher: Bentham Open
                ISSN (Electronic): 1874-3579
                Publication date (Electronic): 28 February 2018
                Publication date Collection: 2018
                Volume: 12
                Pages: 16-25
                Affiliations
                [1 ]Department of Public Health and Infectious Diseases, “Sapienza” University of Rome, Rome, Italy
                [2 ]Department of Molecular Medicine, Laboratory of Virology, “Sapienza” University of Rome, Rome, Italy
                [3 ]Virology and Molecular Biology Unit, Department of Diagnostic Pathology, Istituto Nazionale Tumori, IRCCS Fondazione G. Pascale, Naples, Italy
                Author notes
                [* ]Address correspondence to this author at the Department of Public Health and Infectious Diseases, “Sapienza” University of Rome, Rome, Italy; Tel: +393896943773; E-mail: giuseppe.coranoscheri@ 123456uniroma1.it
                Article
                Publisher ID: TOVJ-12-16
                DOI: 10.2174/1874357901812010016
                PMC ID: 5842384
                PubMed ID: 29541275
                SO-VID: 7031e1f3-d280-4828-8ddd-b249fdfb7307
                Copyright © © 2018 Schietroma et al.
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution 4.0 International Public License (CC-BY 4.0), a copy of which is available at: https://creativecommons.org/licenses/by/4.0/legalcode. This license permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                History
                Date received : 28 August 2017
                Date revision received : 26 September 2017
                Date accepted : 02 February 2018
                Categories
                Subject: Virology
                Series title: Suppl-1, M2

                ScienceOpen disciplines: Microbiology & Virology
                Keywords: hcv,hcc,daa’s,immunity,viral factors,chronic infection
                Data availability:
                ScienceOpen disciplines: Microbiology & Virology
                Keywords: hcv, hcc, daa’s, immunity, viral factors, chronic infection

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