AIM:In recent years,studies have suggested that Epstein-Barr virus(EBV)is associated with HCC.The present studywas to determine the prevalence of EBV in HCC patients,and whether EBV acted synergistically with hepatitis virusesin HCC carcinogenesis.METHODS:Liver tissue 115 HCC patients and 26 non-carcinoma patients were studied.Polymerase chain reaction(PCR)was performed to detect EBV BamHI W DNA,EBVLMP1 DNA,HBV X DNA,and HBV S DNA.Reverse transcriptionPCR(RT-PCR)was performed to detect HCV RNA and HDVRNA.Immunohistochemistry was performed to detect LMP1,HBsAg,HBc_Ag and HCV.The positive ratios were comparedbetween HCC group and control group by X~2 test.RESULTS:Totally,78 HCC samples whose β-globulin DNAwas positively detected by amplified PCR were selected.PCR was performed in all cases for EBV DNA and HBV DNA.RT-PCR was performed in 18 cases for HCV RNA and HDVRNA.EBV BamHI W and EBV LMP1 were positive in 18 and 6cases,respectively.HBV X gene and HBV S gene were positivein 42 and 27 cases respectively.HCV was positive in oneof the 18 cases,and none was positive for HDV.The positiverates were 28.2%(22 of 78)for EBV DNA(BamHI W and/orLMP1)and 56.4%(44 of 78)for HBV DNA(X gene and/orS gene)respectively.In addition,12 cases were positivefor both EBV DNA and HBV DNA.Among the 26 cases in thecontrol group,2 cases were positive for EBV BamHI W,4positive for HBV X gene and 3 positive for HBV S gene.Thepositive rates were 8.0%(2 of 26)and 23.1%(6 of 26),respectively,for EBV DNA and HBV DNA.The result of DNAsequencing of BamHI W was 100% homologous with thecorresponding sequence of B95-8.There was significantdifference in EBV infection rate between HCC patients andcontrols(x~2=4.622,P<0.05).The difference in HBV infectionrate was also significant(x~2 8.681,P<0.05).However,therewas no obvious correlation between HBV and EBV in HCCpatients(x~2=0.835,P>0.05).LMP1,HBV(HBsAg,HBcAg)and HCV were detected positively in 25,45 and 6 of 78 cases of HCC tissues respectively.In the 26 control cases,the corresponding positive cases were 2,4 and O.Thedifference in EBV infection rate between HCC patientsand control cases was statistically significant(x~2=6.02,P<0.05).The difference in HBV infection rate was alsostatistically significant(x~2=10.03,P<0.05).In the 25 caseswith positive LMP1 expression,6 were in the nuclei of tumorcells,9 in the cytoplasm of tumor cells and 10 in mesenchymallymphocyte cytoplasm.CONCLUSION:The existence of EBV infection in HCC tissuessuggests that EBV may be involved in the hepatocellularcarcinogenesis in China.HBV infection may be a majorcause of HCC.There is no correlation between EBV andHBV in the development of HCC.The prevalence of HCVinfection is low in our area,and HDV appears not to play adirect role in hepatocellular carcinogenesis. AIM: In recent years, studies have suggested that Epstein-Barr virus (EBV) is associated with HCC. The present study was determining the prevalence of EBV in HCC patients, and whether EBV acted synergistically with hepatitis viruses in HCC carcinogenesis. METHODS: Liver tissue 115 HCC patients and 26 non-carcinoma patients were studied. Polymerase chain reaction (PCR) was performed to detect EBV BamHI W DNA, EBVLMP1 DNA, HBV X DNA, and HBV S DNA. HCV RNA and HDV RNA. Immunohistochemistry was performed to detect LMP1, HBsAg, HBc_Ag and HCV. The positive ratios were more than HCC group and control group by X ~ 2 test. RESULTS: Totally, 78 HCC samples whose β-globulin DNA was positively detected by amplified PCR were selected in all cases for EBV DNA and HBV DNA. RT-PCR was performed in 18 cases for HCV RNA and HDV RNA. EBV BamHI W and EBV LMP1 were positive in 18 and 6 cases, respectively. HBV X gene and HBV S gene were positivein 42 and 27 EBV DNA (BamHI W and / or LMP1) and 56.4% (44 of 78) for HBV DNA were positive for each of the 18 cases, and none was positive for one of the 18 cases, (X gene and / or S gene) respectively. In addition, 12 cases were positive for both EBV DNA and HBV DNA. Among the 26 cases in the control group, 2 cases were positive for EBV BamHI W, 4 positive for HBV X gene and 3 positive for HBV S gene.Thepositive rates were 8.0% (2 of 26) and 23.1% (6 of 26), respectively, for EBV DNA and HBV DNA.The result of DNA sequencing of BamHI W was 100% homologous with the response sequence of B95-8 There was a significant difference between the EBV infection rate between HCC patients and controls (x 2 = 4.622, P <0.05). The difference in HBV infection was also significant (x ~ 2 8.681, P <0.05) HBV and EBV in HCC patients (x 2 = 0.835, P> 0.05) .LMP1, HBV (HBsAg, HBcAg) and HCV were detected in 25, 45 and 6 of 78 cases of HCC tissues respectively.control cases, the corresponding positive cases were 2, 4 and O. Thifference in EBV infection rate between HCC patients and control cases was statistically significant (x ~ 2 = 6.02, P <0.05). The difference in HBV infection rate was alsostatistically significant ~ 2 = 10.03, P <0.05) .In the 25 cases with positive LMP1 expression, 6 were in the nuclei of tumor cells, 9 in the cytoplasm of tumor cells and 10 in mesenchymallymphocyte cytoplasm. CONCLUSION: The existence of EBV infection in HCC tissuessuggests that EBV may be involved in the hepatocellularcarcinogenesis in China. HBV infection may be a major cause of HCC. There is no correlation between EBV and HBV in the development of HCC. Prevalence of HCV infection is low in our area, and HDV appears not to play an adirect role in hepatocellular carcinogenesis.