Innate and Adaptive Immunopathogeneses in Viral Hepatitis; Crucial Determinants of Hepatocellular Carcinoma
Viral hepatitis B (HBV) and hepatitis C (HCV) infections remain the most common risk factors for the development of hepatocellular carcinoma (HCC), and their heterogeneous distribution influences the global prevalence of this common type of liver cancer. Typical hepatitis infection elicits various i...
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| Veröffentlicht in: | Cancers 2022-02, Vol.14 (5), p.1255 |
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| creator | Zaki, Marco Y W Fathi, Ahmed M Samir, Samara Eldafashi, Nardeen William, Kerolis Y Nazmy, Maiiada Hassan Fathy, Moustafa Gill, Upkar S Shetty, Shishir |
| description | Viral hepatitis B (HBV) and hepatitis C (HCV) infections remain the most common risk factors for the development of hepatocellular carcinoma (HCC), and their heterogeneous distribution influences the global prevalence of this common type of liver cancer. Typical hepatitis infection elicits various immune responses within the liver microenvironment, and viral persistence induces chronic liver inflammation and carcinogenesis. HBV is directly mutagenic but can also cause low-grade liver inflammation characterized by episodes of intermittent high-grade liver inflammation, liver fibrosis, and cirrhosis, which can progress to decompensated liver disease and HCC. Equally, the absence of key innate and adaptive immune responses in chronic HCV infection dampens viral eradication and induces an exhausted and immunosuppressive liver niche that favors HCC development and progression. The objectives of this review are to (i) discuss the epidemiological pattern of HBV and HCV infections, (ii) understand the host immune response to acute and chronic viral hepatitis, and (iii) explore the link between this diseased immune environment and the development and progression of HCC in preclinical models and HCC patients. |
| doi_str_mv | 10.3390/cancers14051255 |
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Typical hepatitis infection elicits various immune responses within the liver microenvironment, and viral persistence induces chronic liver inflammation and carcinogenesis. HBV is directly mutagenic but can also cause low-grade liver inflammation characterized by episodes of intermittent high-grade liver inflammation, liver fibrosis, and cirrhosis, which can progress to decompensated liver disease and HCC. Equally, the absence of key innate and adaptive immune responses in chronic HCV infection dampens viral eradication and induces an exhausted and immunosuppressive liver niche that favors HCC development and progression. The objectives of this review are to (i) discuss the epidemiological pattern of HBV and HCV infections, (ii) understand the host immune response to acute and chronic viral hepatitis, and (iii) explore the link between this diseased immune environment and the development and progression of HCC in preclinical models and HCC patients.</description><identifier>ISSN: 2072-6694</identifier><identifier>EISSN: 2072-6694</identifier><identifier>DOI: 10.3390/cancers14051255</identifier><identifier>PMID: 35267563</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Adaptive immunity ; Carcinogenesis ; Chronic infection ; Cirrhosis ; Comorbidity ; Epidemiology ; Fibrosis ; Genomes ; Heparan sulfate ; Hepatitis B ; Hepatitis C ; Hepatocellular carcinoma ; Immune response ; Immunotherapy ; Infections ; Inflammation ; Liver cancer ; Liver cirrhosis ; Liver diseases ; Malignancy ; Microenvironments ; Mortality ; Proteins ; Review ; Risk factors ; Vaccines ; Viral infections ; Viruses</subject><ispartof>Cancers, 2022-02, Vol.14 (5), p.1255</ispartof><rights>2022 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). 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The objectives of this review are to (i) discuss the epidemiological pattern of HBV and HCV infections, (ii) understand the host immune response to acute and chronic viral hepatitis, and (iii) explore the link between this diseased immune environment and the development and progression of HCC in preclinical models and HCC patients.</description><subject>Adaptive immunity</subject><subject>Carcinogenesis</subject><subject>Chronic infection</subject><subject>Cirrhosis</subject><subject>Comorbidity</subject><subject>Epidemiology</subject><subject>Fibrosis</subject><subject>Genomes</subject><subject>Heparan sulfate</subject><subject>Hepatitis B</subject><subject>Hepatitis C</subject><subject>Hepatocellular carcinoma</subject><subject>Immune response</subject><subject>Immunotherapy</subject><subject>Infections</subject><subject>Inflammation</subject><subject>Liver cancer</subject><subject>Liver cirrhosis</subject><subject>Liver diseases</subject><subject>Malignancy</subject><subject>Microenvironments</subject><subject>Mortality</subject><subject>Proteins</subject><subject>Review</subject><subject>Risk factors</subject><subject>Vaccines</subject><subject>Viral infections</subject><subject>Viruses</subject><issn>2072-6694</issn><issn>2072-6694</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpdUU1LAzEQDaLYUj17k4Dn2uxmk-wiCKV-FQpe1GtIs7Nt6m6yJtmC_94traLOZYaZN2_e8BC6SMg1pQWZaGU1-JBkhCUpY0domBKRjjkvsuNf9QCdh7AhfVCaCC5O0YCylAvG6RC9z61VEbCyJZ6Wqo1mC3jeNJ11rYprtwILAQI2Fr8Zr2r8BH3fRBNu8Mx32vStO4jgG2OVjQG7ag9xGuq6q5XHM-W1sa5RZ-ikUnWA80MeodeH-5fZ03jx_DifTRdjneUijgsh8rwkuuI6FYKwtNBVpXr5vCwTAOA0hXJJsmT3BWc5IxkHlWuaAdBlXtARut3ztt2ygVKDjb1y2XrTKP8pnTLy78SatVy5rcwLUgi2I7g6EHj30UGIcuM6b3vNMuVU8IQWWdajJnuU9i4ED9XPhYTInUHyn0H9xuVvYT_4bzvoF51Pj1k</recordid><startdate>20220228</startdate><enddate>20220228</enddate><creator>Zaki, Marco Y W</creator><creator>Fathi, Ahmed M</creator><creator>Samir, Samara</creator><creator>Eldafashi, Nardeen</creator><creator>William, Kerolis Y</creator><creator>Nazmy, Maiiada Hassan</creator><creator>Fathy, Moustafa</creator><creator>Gill, Upkar S</creator><creator>Shetty, Shishir</creator><general>MDPI AG</general><general>MDPI</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7T5</scope><scope>7TO</scope><scope>7XB</scope><scope>8FE</scope><scope>8FH</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-0734-5007</orcidid><orcidid>https://orcid.org/0000-0002-1291-1413</orcidid><orcidid>https://orcid.org/0000-0002-4729-2173</orcidid><orcidid>https://orcid.org/0000-0003-3097-5776</orcidid></search><sort><creationdate>20220228</creationdate><title>Innate and Adaptive Immunopathogeneses in Viral Hepatitis; 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| subjects | Adaptive immunity Carcinogenesis Chronic infection Cirrhosis Comorbidity Epidemiology Fibrosis Genomes Heparan sulfate Hepatitis B Hepatitis C Hepatocellular carcinoma Immune response Immunotherapy Infections Inflammation Liver cancer Liver cirrhosis Liver diseases Malignancy Microenvironments Mortality Proteins Review Risk factors Vaccines Viral infections Viruses |
| title | Innate and Adaptive Immunopathogeneses in Viral Hepatitis; Crucial Determinants of Hepatocellular Carcinoma |
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