Article Sidebar
Published:
Nov 24, 2016Article Details
Copyright remains in the Author’s name. The work is licensed under a Creative Commons Attribution - Noncommercial Works License. Authors are required to complete and sign an Author Agreement form that outlines Author and Publisher rights and terms of publication. The Agreement form should be uploaded along with other submissions files and any submission will be considered incomplete without it [forthcoming].
Material submitted for publication in the SAMJ is accepted provided it has not been published or submitted for publication elsewhere. Please inform the editorial team if the main findings of your paper have been presented at a conference and published in abstract form, to avoid copyright infringement. The SAMJ does not hold itself responsible for statements made by the authors.
Previously published images
If an image/figure has been previously published, permission to reproduce or alter it must be obtained by the authors from the original publisher and the figure legend must give full credit to the original source. This credit should be accompanied by a letter indicating that permission to reproduce the image has been granted to the author/s. This letter should be uploaded as a supplementary file during submission.
Main Article Content
Hepatitis viruses and hepatocellular carcinoma
Abstract
Of the hepatitis viruses that have been identified and their pathological consequences characterised, three - hepatitis B virus (HBV), hepatitis C virus (HCV) and hepatitis D virus (HDV) - have been implicated as risk factors for hepatocellular carcinoma (HCC) in humans. Sufficient evidence is now available to justify the conclusions that chronic infection with HBV and HCV, but not HDV, are causes of HCC. Hepatocellular carcinogenesis is a complex step-wise process that evolves over many years, and the precise way(s) in which these two viruses induce malignant transformation remain uncertain. The observation that HBV DNA is integrated into cellular DNA in the great majority of, and perhaps all, HBV-related HCCs, whereas replicative intermediates of HCV do not insert into host DNA in HCVrelated HCC, makes it very likely that different pathogenic mechanisms operate in HBV- and HCV-induced HCC. Indeed, evidence is mounting that both direct and indirect mechanisms, and often the two together, are involved in the genesis of HBV-related HCC, but that HCV appears only to induce HCC indirectly by causing chronic necroinflammatory hepatic disease which in turn is responsible for tumour formation. There is some evidence that the two viruses may interact in the development of HCC, but this remains to be proven. Animal models - other members of the hepadnavirus family (to which HBV belongs) that also cause HCC in their respective animal hosts, and transgenic mice into which sequences of HBV DNA have been inserted - are proving useful in elucidating putative mechanisms of HBV-related hepatocellular carcinogenesis, but no models for studying HCV-induced HCC are yet available. Whatever the pathogenesis of HBV-induced and HCV-induced HCC, the viruses do not act alone but in conjunction with other environmental carcinogens and a number of host factors.
