| Background and Aims:Hepatocellular carcinoma (HCC) is one of the most common cancers, which is also the third cause of cancer-related death per year in the world. Hepatitis B virus (HBV) is probably the etiologic agent for52%of HCC. The risk of HCC increases with increasing serum HBV viral load. HBV DNA level is a marker of viral replication and efficacy of antiviral treatment. HBV DNA level correlates with the development of HCC, but the role of viral load in inflammatory tumor microenvironment remains unclear. We aimed to investigate the influence of viral load and antiviral treatment on immune microenvironment of HCC. CD3+, CD4+CD8+, CD68+cells were the major immune cells for antiviral and antitumoral immunity.Methods:From2006to2009,286HBV-related HCC patients who underwent hepatectomy were randomly enrolled.We designed the following three different groups. Group A with HBV DNA level<103copies/ml, never received antiviral treatment before hepatectomy. Group B with HBV DNA>105copies/ml, never received antiviral treatment before hepatectomy. Group C with HBV DNA level<103copies/ml, had received antiviral treatment for at least6months before hepatectomy, HBV DNA>105copies/ml before receiving the antiviral treatment. CD3+, CD4+, CD8+, CD25+, CD68+cells were assessed by immunohistochemistry in tissue microarrays. Results:CD3+, CD4+, CD8+, CD25+, CD68+cells were not associated with disease-free survival (DFS). Peritumoral CD8+CTLs density in group C was lower than in group B (P=0.003). Low peritumoral CD8+CTLs density was an independent prognostic factor for improved overall survival (OS)(P=0.005). The OS of Group C was better than Group B (P<0.001)Conclusions:Antiviral treatment not only reduces HBV DNA level, but also affects peritumoral CD8+CTLs. Peritumoral CD8+CTL is an independent predictor for OS in HCC. |
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