Analysis of HLA-DQB1 gene polymorphisms in asymptomatic HBV carriers and chronic hepatitis B patients in the Chinese Han population

Host genetic factors and environment factors including hepatitis B virus (HBV) genotype are widely viewed as common basis of the different outcomes of HBV infection. Human leucocyte antigen (HLA) plays an important role in immunological reaction to HBV infection. The study aimed to explore whether the HLA-DQB1 allele polymorphisms are associated with the outcomes of HBV infection in the Chinese Han population. One hundred and thirty-four asymptomatic HBV carriers and 139 chronic hepatitis B patients were recruited in this case-control study in Beijing, China. Sequence-specific primers-polymerase chain reaction was used to detect 13 alleles of HLA-DQB1 gene. The frequency distributions of alleles in two groups were analysed using sas 9.1.2 software. After adjustment of confounders the frequencies of HLA-DQB1*0503 allele and *0303 allele in chronic hepatitis B group were statistically significant lower than those in asymptomatic HBV carrier group (P = 0.04; P = 0.05), and the frequency of exposure to alcohol consumption in patients with chronic hepatitis B was clearly higher than that in asymptomatic HBV carrier group (P = 0.004). HLA-DQB1*0503 allele and *0303 allele are independently resistant genetic factors to chronic hepatitis B, and alcohol consumption is the risk factor of chronic hepatitis B.     

Clinical characteristics and chronicity of acute hepatitis B induced by lamivudine-resistant strains

Whether resistant hepatitis B virus (HBV) strains are transmissible and can lead to chronic infection remains to be studied. The aim of this study was to investigate the clinical characteristics of patients with acute hepatitis B caused by lamivudine (LAM)‐resistant strains. Sera were collected from 234 Chinese patients with acute hepatitis B. LAM‐resistance mutations were identified by direct polymerase chain reaction (PCR) sequencing. LAM‐resistant HBV variants were detected in 11 of the 234 (4.7%) patients. Among these patients, six harbored the rtM204I mutation, two harbored the rtL180M + rtM204I mutations, one harbored the rtM204I + rtM204V mutations, one harbored the rtL80I + rtM204I mutations, and one harbored the rtV173L + rtL180M + rtM204V mutations. Three patients were infected with genotype B HBV and eight patients were infected with genotype C HBV. Two patients infected with viruses with LAM‐resistance mutations developed severe acute hepatitis. One patient developed chronic hepatitis B. This patient was infected with genotype C HBV that had LAM‐resistance mutations (rtL180M + rtM204I). The patient was diagnosed with an occult hepatitis B virus infection based on the presence of HBV DNA in the liver and the absence of detectable hepatitis B surface antigen (HBsAg) in the serum. LAM‐resistant HBV strains in China are transmissible, can cause acute hepatitis B, and can even progress to chronic infection in China. J. Med. Virol. 84:1558–1561, 2012. © 2012 Wiley Periodicals, Inc.     

HLA-DRB1*10与中国人慢性乙肝关联

目的研究ＨＬＡ－ＤＲＢ１基因与乙肝的关联,探讨可能由病毒感染继发的自身免疫反应导致疾病发展的主要原因,为乙肝的病因学及预后估计提供免疫学方面的资料。方法在我国北方地区随机选择５４名慢性乙肝患者,用ＰＣＲ／ＳＳＰ方法进行ＨＬＡ－ＤＲＢ１等位基因分型,对照组为同地区９２名健康人。采用疾病和ＨＬＡ相关分析软件进行数据处理。结果病人组ＨＬＡ－ＤＲＢ１＊１０基因频率明显增高为２５．９％（ＲＲ＝１０．３８,Ｐｃ＝０．００１）,其它等位基因频率在实验组与对照组间差异无显著性。结论ＨＬＡ－ＤＲＢ１＊１０基因与中国北方人群慢性乙肝关联     

HBV基因型与HBV感染慢性化、重症化的关系

目的 探讨HBV基因型与HBV感染后慢性化、重症化的关系.方法 应用型特异性引物聚合酶链反应法,对中国2922例HBV感染者进行HBV基因型检测,比较各临床类型HBV感染者基因型分布差异及各基因型HBV感染者肝功能和病毒学差异.结果 2922例HBV感染者中,基因型B、C、B/C、D分别占15.9%、83.5%、0.41%、0.21%.与慢性肝炎比较急性肝炎B基因型所占比例较高（P=0.003）,肝硬化和肝细胞性肝癌C基因型所占比例较高（P值均为0.000）,慢加急性肝衰竭与慢性肝炎比较基因型分布差异无统计学意义.急性肝炎和慢性肝炎B、C基因型患者HBeAg 阳性率、HBV DNA病毒载量、肝功能生化指标差异无统计学意义.慢加急性肝衰竭、肝硬化、肝细胞性肝癌组C基因型较B基因型患者HBeAg阳性率更高（P值分别为0.000、0.024、0.003）,肝细胞性肝癌C基因型患者HBV DNA病毒载量高于B基因型患者（P=0.025）,慢加急性肝衰竭和肝细胞性肝癌组C基因型较B基因型患者胆碱酯酶更低（P值为0.0004、0.02）.结论 中国HBV感染者的HBV基因型以B、C基因型为主,少量的B/C、D基因型;C基因型较B基因型HBV感染者更易发生慢性化和进展为肝硬化和肝细胞性肝癌,但未观察到基因型对慢加急性肝衰竭发生的差异.急性和轻症HBV感染者B、C基因型未显示对病情的明显影响,但重症和终末期HBV感染者C基因型较B基因型患者HBeAg阳性率、HBV DNA病毒载量更高,肝功能损害更严重.     

HLA-DQA1基因多态性和HBV感染结局的关联

目的 探讨人类白细胞抗原(HLA)DQA1基因多态性与乙型肝炎病毒(HBV)感染临床结局的关联.方法 临床收集慢性乙型肝炎(120例)、慢性HBV携带者(60例)、自限性HBV感染者(60例)三组病例,前两组诊断均经肝活检证实.聚合酶链反应序列特异性引物(PCR-SSP)法检测HLA-DQA1基因型,比较组间基因频率的差异.结果 (1)HLA-DQA1*0201在慢性乙型肝炎组的分布频率显著高于自限性HBV感染组(38.3% vs 5.8%,P<0.001,A=10.04,95% CI:4.48～22.48);HLA-DQA1*0102的分布频率显著低于自限性HBV感染组(9.6% vs 36.7%,P<0.001,A=0.183,95%CI:0.10～0.32).(2)HLA-DQA1*0201在慢性乙型肝炎组的分布频率显著高于慢性HBV携带者组(38.3% vs 7.5%,P<0.01,A=7.667,95% CI:3.7～15.87);HLA-DQA1*0102的分布频率显著低于慢性HBV携带者(20% vs 9.6%.P<0.01,A=0.424,95% CI:0.23～0.79).结论 HLA-DQAI基因多态性影响HBV感染临床结局,其中DQA1*0102呈保护作用,DQA1*0201可能促进HBV感染的慢性化和肝炎的发生.     

Distribution of hepatitis B virus in the liver of chronic hepatitis C patients with occult hepatitis B virus infection

Although occult hepatitis B virus (HBV) infection (HBV-DNA in serum in the absence of hepatitis B surface antigen [HBsAg]) is common in chronic hepatitis C, its characteristics are not well known. In this work, the presence of HBV-DNA (by polymerase chain reaction; PCR) and its distribution (by in situ hybridization) in liver biopsies and peripheral blood mononuclear cells (PBMCs) from 32 patients with chronic hepatitis C and occult HBV infection and in 20 HBsAg chronic carriers were determined. The results showed that serum HBV-DNA levels were statistically lower (P = 0.001) in patients with occult HBV infection than in HBsAg chronic carriers. The HBV infection pattern in liver cells was identical between patients with occult HBV infection and those with chronic hepatitis B. However, the mean percentage of HBV-infected hepatocytes was significantly lower (P = 0.001) in patients with occult HBV infection (5 +/- 4.44%) than in HBsAg chronic carriers (17.99 +/- 11.58%). All patients with chronic hepatitis B have HBV-DNA in their PBMCs while this occurred in 50% of the cases with occult HBV infection. In conclusion, patients with occult HBV infection have a low number of HBV-infected hepatocytes and this fact could explain the lack of HBsAg detection and low viremia levels found in these cases.     

Acute and chronic hepatitis delta virus infection: Direct or indirect effect on hepatitis B virus replication?

In a large population of patients, chronic hepatitis delta virus (HDV) infection was usually associated with absence of hepatitis B virus (HBV) replication. However, acute HDV superinfection progressing to chronic HDV infection in two hepatitis B e antigen (HBeAg)-positive HBV carriers and coinfection in two other patients who progressed to chronic HBV (HBeAg-positive) and HDV infection was associated with continuing high-level HBV replication for several years. Thus HDV infection does not always inhibit HBV replication. The hypothesis that the different effects of HDV coinfection and superinfection on HBV replication may stem from variability in the capacity of the host to produce and respond to interferon is discussed.     

白细胞介素10基因启动子区多态性与乙型肝炎病毒感染预后的关联研究

目的探讨中国汉族人白细胞介素10基因(interleukin10gene,IL10)启动子区单核苷酸多态性与乙型肝炎病毒(hepatitisBvirus,HBV)感染、转归的关联。方法采用聚合酶链反应-限制性片段长度多态性分析方法,检测231例HBV感染者,165例HBV感染康复者和135名正常对照者IL10基因启动子-1082G/A、-819T/C、-592A/C位点基因型。结果IL10基因启动子-1082G/A、-819T/C、-592A/C位点基因型和等位基因在HBV感染组、HBV感染康复组和正常对照组之间的分布频率比较差异无统计学意义(P>0.05),在血清HBV-DNA<1×103拷贝/mL的HBV感染者组和HBV-DNA≥1×103拷贝/mL组之间的分布频率比较差异亦无统计学意义(P>0.05);但IL10基因启动子-819T/C和-592A/C位点基因型和等位基因在HBV无症状携带组和慢性乙型肝炎组之间的分布差异有统计学意义(P<0.05),-819T/C位点TT型和-592A/C位点AA型在慢性乙型肝炎组的频率明显较高。结论汉族人IL10基因启动子多态性可能与人群对HBV易感性及感染后的病毒血症水平无显著相关性;但IL10启动子-819T/C和-592A/C位点基因多态性与HBV感染后的肝脏炎症反应有关。     

维生素D受体基因多态性与乙型肝炎病毒感染的关联研究

目的探讨中国汉族人群维生素D受体（vitamin D receptor，VDR）基因多态性是否与乙型肝炎病毒（hepatitis B virus，HBV）感染结局相关联。方法以184例慢性乙肝患者和205名无症状HBV携带者为研究对象，收集外周血，提取基因组DNA，应用聚合酶链反应．限制性片段长度多态性（polymerase chain reaction-restriction fragmentlength polymorphism，PCIR-RFLP）方法，分析VDR基因第2外显子Fok Ⅰ位点、第9外显子Taq Ⅰ位点的多态性分布。结果单因素分析结果显示Fok Ⅰ位点FF基因型在慢性乙肝组的频率44．6％显著高于无症状HBV携带组的31．7％（P〈0．05）。经多因素非条件Logistic回归分析调整混杂作用后，结果仍然显示FF基因型在慢性乙肝组与无症状HBV携带组之间的差异存在统计学意义（OR=1．95，P〈0．05）。FokⅠ位点与TapⅠ位点组成的FT单倍型在慢性乙肝组的分布频率显著高于无症状HBV携带组（OR=1．45，P〈0．05），fT单倍型在慢性乙肝组的分布频率显著低于无症状HBV携带组（OR=0．72，P〈0．05）。结论维生素D受体基因多态性可能影响HBV感染的遗传易感性。     

Hepatitis B virus (HBV) subgenotypes C2 and B2 differ in lamivudine- and adefovir-resistance-associated mutational patterns in HBV-infected Chinese patients

We aimed to study the prevalence and clinical implications of hepatitis B virus (HBV) subgenotypes in Chinese patients. A total of 4,300 patients, mainly from northern China, were enrolled, including 182 patients with acute hepatitis B and 4,118 patients with chronic HBV infection who had been exposed to nucleoside or nucleotide analogs. HBV genotypes/subgenotypes were determined by direct sequencing of the HBV S/Pol region. The prevalence rates were 0.40% for HBV/B1, 14.30% for HBV/B2, 0.25% for HBV/B3, 0.35% for HBV/B4, 1.05% for HBV/C1, 81.72% for HBV/C2, 0.93% for HBV/C3, 0.16% for HBV/C4, and 0.84% for HBV/D. In chronic HBV infection, patients with HBV/B2 were younger and had lower ΗBeAg positive rates than patients with HBV/C2. The incidence of lamivudine-resistant mutations was significantly higher in HBV/C2 compared to HBV/B2 (27.9% versus 19.8%; P<0.01), and the significant difference was observed only for rtM204I and not rtM204V. In addition, compensatory mutations were more frequently detected in HBV/C2. The incidence of adefovir-resistant mutations was similar between the two subsets, but HBV/C2 inclined to show rtA181V (3.6% for C2 versus 0.9% for B2; P<0.01), while HBV/B2 inclined to show rtN236T (4.5% for versus 2.5% for C2; P<0.01). The ratios of HBV/B2 to HBV/C2 infection were 1.7 (110/65), 5.7 (2,653/463), 7.5 (520/69), 8.0 (48/6), and 15.3 (183/12) for acute hepatitis B, chronic hepatitis B, liver cirrhosis, acute-on-chronic liver failure, and hepatocellular carcinoma, respectively. In conclusion, HBV/C2 and HBV/B2, two prevalent subgenotypes, differ in lamivudine- and adefovir-resistance-associated mutational patterns. HBV/C2-infected patients are more likely to have disease progression than HBV/B2-infected ones.     

TT virus infection in patients with chronic hepatitis B or C: influence on clinical, histological and virological features

Concomitant infection with TT virus and hepatitis B virus (HBV) or hepatitis C virus (HCV) is common. However, the effect of TTV infection on chronic hepatitis B or C is unknown. The prevalence of TTV infection, the effect of TTV infection on the clinical, histological and virological features of patients with chronic hepatitis B or C, and the influence of TTV infection on the HCV response to interferon alfa therapy were studied. A total of 100 asymptomatic hepatitis B surface antigen carriers, 220 patients with HBV-related chronic liver diseases, and 110 patients with chronic hepatitis C treated with interferon alfa (3 million units subcutaneously three times a week for 24 weeks) were enrolled. Serum HCV RNA and serum TTV DNA were detected by the polymerase chain reaction (PCR). Serum HBV DNA and serum HCV RNA level were quantified by branched DNA assays. Infection with TTV was detected in 21.5% of HBV carriers and 37% of HCV carriers. TTV infection had little effect on the clinicopathological course of chronic HBV infection. In chronic hepatitis C, clinical features, histological severity, serum HCV RNA levels, and the response to interferon alfa therapy did not differ between those with and without TTV infection. The loss of serum TTV DNA did not correlate with the biochemical response as did in the loss of serum HCV RNA. In conclusion, TTV infection is found frequently in patients with chronic hepatitis B or C in Taiwan; however, coinfection with TTV does not affect the clinicopathological course of chronic hepatitis B or C and the response to interferon alfa therapy.     

Response of pre-core mutant chronic hepatitis B infection to lamivudine

The proportion of chronic liver disease associated with the pre-core mutant of hepatitis B virus (HBV) infection is increasing, particularly in Mediterranean Europe and in Asia. The pre-core mutant HBV is unable to produce hepatitis B e antigen (HBeAg), so that patients with this variant do not present with HBV characterised by HBeAg in the serum. Pre-core mutant chronic hepatitis B infection usually proceeds to serious liver disease. Wild-type HBV infection may be mild and respond relatively well to interferon (IFN) alpha therapy, but IFN alpha is not an effective therapeutic option in pre-core mutant hepatitis B infection and new therapeutic options are needed. Clinical data show that lamivudine is an effective treatment for patients with pre-core mutant hepatitis B. There is profound suppression of HBV replication and improvement in indicators of liver disease in most patients. In conclusion, lamivudine is suitable for treatment of a wide range of patients with chronic hepatitis B, including those with pre-core mutant HBV infection.     

HLA-DRB1及HLA-DQA1单倍型与乙型肝炎病毒感染结局的关联研究

目的探讨中国北方汉族人群HLA-DRB1、DQA1单倍型与乙型肝炎病毒（hepatitis B virus，HBV）感染不同结局的关系。方法采用序列特异性引物聚合酶链反应（sequence specific primers polymerase chain reaction，PCR-SSP）技术检测HLA-DRB1、DQA1等位基因，并比较207例慢性乙型肝炎患者，212名无症状HBV慢性携带者（HBV携带者），148例自限性HBV感染者的单倍型频率。结果自限性HBV感染组单倍型DRB1＊04-DQA1＊0301的频率为10．03％，显著高于慢性乙肝组的3．66％（P=0．0005）：DRB1＊15／＊16-DQA1＊0102的频率为6．80％，显著高于慢性乙肝组的1．94％（P=0．0012）和无症状HBV慢性携带者组的1．65％（P=0．004）；DRB1＊04-DQA1＊0302单倍型在慢性乙型肝炎组的频率为3．10％，明显高于自限性HBV感染组的0．39％（P=0．0077）。结论HLA-DRB1、DQA1单倍型与个体感染HBV后的不同结局存在显著关联。     

Hepatitis with isolated serum antibody to hepatitis B core antigen. A variant of non-A, non-B hepatitis?

Antibody to hepatitis B core antigen (anti-HBc) has previously been recognized to be a sensitive marker of hepatitis B virus (HBV) infection. In addition, anti-HBc has recently been suggested to be a surrogate marker for non-A, non-B hepatitis agents in donated blood. The authors studied prospectively the HBV antigen and antibody status in four patients with chronic hepatitis and persistent presence of isolated anti-HBc in their sera. The serologic and histopathologic findings of these four patients were compared with those of three groups of patients having chronic hepatitis with or without HBV markers. A low concentration of serum HBV DNA was detected in only one of the four patients with hepatitis with isolated anti-HBc and in another patient with previous HBV infection. HBV antigens and HBV DNA were not detected in the sera and liver biopsies from the remaining patients with hepatitis with isolated anti-HBc and other patients with hepatitis with or without serologic markers of previous hepatitis A or HBV infection. In contrast, all patients with chronic HBV-associated hepatitis had detectable HBV DNA, hepatitis B surface antigen (HBsAg), and hepatitis B e antigen (HBeAg) in their sera and/or liver biopsies. These findings suggest that chronic hepatitis associated with isolated anti-HBc is a heterogenous pathologic entity. The condition of some of these patients may represent a variant of non-A, non-B hepatitis, whereas the remaining patients are chronic hepatitis B carriers with low serum concentrations of HBV.     

The absence of hepatitis B virus DNA in hepatitis B e antigen positive sera from chronic hepatitis B surface antigen carriers in China

Sera from 20 Chinese patients with chronic hepatitis B were examined for hepatitis B e antigen and hepatitis B virus (HBV) DNA. There was considerable discordance with HBV DNA not being detectable in 10 out of 13 (77%) patients who were hepatitis B e antigen positive. Further testing for anti-HBe and HBV-DNA polymerase activity confirmed the results. Possible reasons for this discordance are discussed but neither hepatitis D (delta) infection nor the acquired immunodeficiency syndrome (AIDS) could be implicated.     

Overt and hidden coinfection with hepatitis B and C viruses in chronic liver disease and porphyria cutanea tarda

The aim of this study was to assess the rate of hepatitis B virus (HBV) and hepatitis C virus (HCV) coinfection ("the coinfection") in chronic liver disease (CLD) and to reveal overt and hidden HBV infection in patients with antibodies to HCV (anti-HCV). A total of 209 untreated patients (64 with chronic hepatitis B, 79 with chronic hepatitis C and 66 with porphyria cutanea tarda (PCT)) were screened for serological markers of HBV and HCV infection in serum by third generation enzyme-linked immunosorbent assay (ELISA) methods and for HBV DNA and HCV RNA in serum by polymerase chain reaction (PCR). The rate of the overt coinfection in chronic hepatitis B was very low (2/64, 3%). However, in chronic hepatitis C, the rate of the hidden coinfection with HBV was relatively high (19/79, 24%); these patients had higher alanine transaminase (ALT) and asparagine transaminase (AST) levels in serum and a more advanced liver disease. In PCT patients, the rates of HBV and HCV infections were the same, 21% (14/66). In the PCT patients infected with HBV or HCV, the rate of the coinfection was 33% (7/21). The PCT patients with the coinfection had a high serum ALT level and the worst histological picture in the liver. The hidden HBV infection was more frequent than the overt one. The possibility of the overt or hidden coinfection in CLD renders a detailed analysis of all serum samples for both viruses mandatory. Vaccination against HBV infection should be offered to anti-HCV-positive individuals as well as to PCT patients not showing antibodies to HBV (anti-HBV).     

The high prevalence of the I27 mutant HBcAg18-27 epitope in Chinese HBV-infected patients and its cross-reactivity with the V27 prototype epitope

HBcAg18-27 (FLPSDFFPSV, V27 epitope) is a dominant HLA-A2-restricted epitope in hepatitis B virus (HBV)-infected patients. So far, the occurrence of the epitope has not been assessed in China, where the prevalence of chronic HBV infection is high. In this report, we sequenced the HBV core gene in 105 Chinese patients with chronic HBV infection. Approximately 93.3% (98/105) of the core genes that were sequenced contained mutations with amino acid substitution at position 27 of the core protein: a mutation from a valine to an isoleucine (V27I). The mutant peptide (FLPSDFFPSI, I27) was found to bind to the HLA-A2 molecule with high affinity and elicit specific cytotoxic T lymphocyte (CTL) responses in acutely infected hepatitis B patients. In CTL assays using I27-specific pentamer staining, the V27 epitope showed a cross-reactive T cell response specific for the I27 epitope, but not vice versa. These findings provide important insights for the design of HBcAg18-27-based vaccines in the future.     

TNFA基因启动子区多态性与HBV感染结局的关联研究

目的 在中国汉族人群中探讨TNFA基因启动子区单核苷酸多态性是否与HBV感染结局相关联。方法 以148例HBV自限性感染者和207例慢性乙肝患者为研究对象，应用聚合酶链反应-限制性片段长度多态性和序列特异性引物-PCR方法对TNFA基因启动子区5个位点，-238G／A、-308G／A、-857C／T、-863C／A和-1031T／C进行基因型分型，用EPI和EH等统计学软件分析各位点等位基因、基因型、单倍型频率及其组问差异。结果 TNFA基因-238位GG基因型在慢性肝炎组的频率显著高于自限性感染组（P=0．02），-857TT基因型的频率在慢性肝炎组显著低于自限性感染组（P=0.02）。TNFA基因-238／-308／-857／-863／-1031组成的单倍型GGCCT的频率在慢性肝炎组显著低于自限性感染组（P=0．03），单倍型GGcAT与GGTAT在慢性肝炎组的频率显著高于自限性感染组（P=0．0001，P=0．004）。结论 TNFA基因启动子区多态性与HBV感染结局显著关联。     

Significance of anti-HBc IgM in the differential diagnosis of viral hepatitis

IgM antibody to hepatitis B core antigen (anti-HBc IgM) as determined by IgM capture immunoassay is generally present in high titer during acute hepatitis B infection. A strong positive reaction for anti-HBc IgM during acute hepatitis is indicative of an acute HBV infection even in hepatitis B surface antigen (HBsAg)-negative patients. With the help of anti-HBc IgM otherwise unidentified HBV infection can be diagnosed in HBsAg-negative patients and an optimal combination of diagnostic tests for acute hepatitis B infection would therefore include assays for both HBsAg and anti-HBc IgM. In the HBsAg carrier with or without chronic liver disease the presence and meaning of anti-HBc IgM is still a matter for discussion. Detection of a weak positive result for anti-HBc IgM in HBsAg-positive patients without a recent history of acute hepatitis cannot always be regarded as a definite marker of recent hepatitis B infection. However. quantitation of the anti-HBc IgM results seems to improve the clinical value of the test. Comparison of the available anti-HBc IgM assays is needed and may well establish a reliable cut-off level that would differentiate acute from chronic hepatitis B and ongoing from resolving hepatitis B in HBsAg-positive patients.     

Comparison of the efficacy of lamivudine and famciclovir in Asian patients with chronic hepatitis B: results of 24 weeks of therapy

Lamivudine therapy improves hepatic necro-inflammatory activity, decreases progression of fibrosis, and suppresses hepatitis B virus (HBV) replication. Famciclovir has also been shown to have some effect in the suppression of HBV replication. The aim of the study was to compare the effect of treatment with lamivudine and famciclovir on serum HBV DNA levels in patients with chronic hepatitis B and to assess safety. A prospective randomised clinical study was carried out on 100 patients with chronic hepatitis B infection (50 patients received lamivudine 100 mg daily and 50 patients received famciclovir 500 mg three times a day for 12 weeks. From the twelfth week onwards, patients were offered lamivudine 100 mg daily up to 48 weeks). Significantly more patients treated by lamivudine than by famciclovir had undetectable HBV DNA levels after 12 weeks of therapy (P < 0.001). The median HBV DNA levels were significantly lower in the lamivudine-treated patients from the second week of treatment onwards (P < 0.001 for all time points up to 12 weeks). At week 16, 4 weeks after the famciclovir treated patients were put on lamivudine, there was no longer any difference in HBV DNA levels between the two groups of patients. Both treatments were well tolerated and no serious adverse events were reported. It was concluded that in Chinese patients with chronic hepatitis B infection, lamivudine achieved effective suppression of HBV DNA levels within 4 weeks of therapy whereas famciclovir had a significantly weaker action.