乙型肝炎病毒基因型与恩替卡韦抗病毒疗效关系

目的探讨乙型肝炎病毒（HBV）基因型与恩替卡韦抗病毒治疗疗效的关系。方法应用聚合酶链反应（PCR）-微板核酸分子杂交-酶联免疫吸附测定（ELISA）法检测103例慢性乙型肝炎（CHB）患者HBV的基因型,给予恩替卡韦（O．5mg／d）抗病毒治疗48周;治疗前、治疗后分别检测肝功能、乙型肝炎5项和HBVDNA定量,同时注意药物不良反应。结果103例CHB患者中感染B基因型者34例,感染C基因型者69例。治疗48周,感染B基因型和C基因型患者丙氨酸转氨酶（ALT）复常、HBVDNA转阴、乙型肝炎病毒e抗原（HBeAg）消失和HBeAg／乙型肝炎病毒e抗体（HBeAb）血清转换差异均无统计学意义（P〉0．05）。结论HBV基因型不影响恩替卡韦抗病毒疗效。     

聚乙二醇干扰素α-2a治疗ALT<2ULN HBeAg阴性慢性乙型肝炎48周临床研究

目的:观察聚乙二醇干扰素α-2a治疗ALT<2ULN和肝组织学炎症活动度≥G2的HBeAg阴性慢性乙型肝炎患者的疗效.方法:采用随机、开放、对照的方法,33例ALT<2ULN肝组织学炎症≥G2的HBeAg阴性慢性乙肝分为聚乙二醇干扰素α-2a组16例和恩替卡韦对照组17例,分别接受48周的治疗.治疗24周、48周进行评估.结果:治疗48周,聚乙二醇干扰素α-2a组和恩替卡韦组血清HBV DNA阴转率分别是68.8%和76.7%,比较差异无统计学意义(P>0.05),两组血清HBV DNA水平与基线相比,分别下降(2.71±1.43)lg copies/mL和(2.88±1.03)lg copies/mL,差异无统计学意义(P>0.05).聚乙二醇干扰素α-2a组有1例HBsAg阴转,恩替卡韦组没有1例HBsAg阴转或血清转换.成对活检患者,聚乙二醇干扰素α-2a组和恩替卡韦组肝组织学改善分别是37.5%和60.0%,两组差异具有统计学意义(P<0.05).聚乙二醇干扰素α-2a组治疗后肝组织内HBsAg、HBcAg量明显减少,两组差异无统计学意义(P>0.05).结论:聚乙二醇干扰素α-2a治疗ALT<2 ULN且肝组织学检查≥G2的HBeAg阴性慢性乙型肝炎患者可获得良好的病毒学应答和组织学改善.     

恩替卡韦治疗慢性乙型肝炎的近期疗效

目的研究恩替卡韦（ETV）治疗慢性乙型肝炎（CHB）的近期疗效和安全性。方法85例HBeAg阳性患者随机均分为治疗组（40例）口服ETV（中美上海施贵宝制药有限公司出品）0．5mg／（次·d）,疗程6个月。对照组（45例）采用基因重组干扰素b（IFNb,赛若金,深圳科兴生物工程有限公司生产）500万单位皮下注射或肌肉注射,隔日1次,疗程6个月。结果治疗组8周时HBV-DNA水平较治疗前显著下降;治疗12、24周时,治疗组与对照组HBeAg阳性患者HBV—DNA转阴率、HBeAg阴转率有显著性差异（P〈0．05）。治疗组与对照组谷丙转氨酶（ALT）复常率无显著性差异（P〉0．05）。结论恩替卡韦治疗慢性乙型肝炎,HBV．DNA转阴率、HBeAg阴转率优于干扰素。恩替卡韦治疗过程中未发生与观察药物相关的严重不良反应,患者耐受性较好。     

恩替卡韦治疗HBeAg阳性和阴性慢性乙肝疗效的比较

目的探讨恩替卡韦对HBeAg阳性和阴性慢性乙肝治疗疗效的比较。方法本案选择60铆浸性乙型肝炎患者，其中HBeAg阳性32例，HBeAg阴性28例，均予恩替卡韦0．5mg／d治疗48周。结果经48周治疗后，HBeAg阳性组HBV-DNA转阴率为71％，ALT复常率为65％，HBeAg阴性组HBV-DNA转阴率为85％，ALT复常率为75％，经方差分析两组数据，两组HBV-DNA转阴率和ALT复常率均无显著差异（P〉0．05）。结论恩替卡韦治疗HBeAg阴性的慢性乙肝患者的疗效和HBeAg阳性慢性乙肝患者疗效无显著差异，同样有良好的疗效。     

恩替卡韦联合聚乙二醇干扰素治疗慢性乙型肝炎患者的疗效分析

目的探讨恩替卡韦联合聚乙二醇干扰素治疗对慢性乙型肝炎(CHB)患者的谷丙转氨酶(ALT)复常率、乙型肝炎E抗原(HBeAg)转阴率及乙型肝炎E抗体(HBeAb)转换率的影响。方法选取120例CHB患者均分为2组,均予以基础治疗,对照组采用聚乙二醇干扰素治疗,观察组采用恩替卡韦联合聚乙二醇干扰素治疗。观察并比较2组患者治疗后不同时点的ALT复常率、HBeAg转阴率、HBeAb转换率、病毒学突破率及治疗期间不良反应发生情况。结果观察组临床疗效总有效率显著高于对照组(P 0. 05);治疗6、12、24周后,2组血清ALT水平均较治疗前显著改善(P 0. 05),但2组间血清ALT水平差异无统计学意义(P 0. 05);治疗12、24周后,观察组ALT复常率、HBeAg转阴率、HBeAb转换率均显著高于对照组(P 0. 05);观察组治疗12、24周后病毒学突破率均显著低于对照组(P 0. 05); 2组治疗24周后Th1/Th2型细胞因子水平均较治疗前显著改善(P 0. 05);观察组治疗24周后INF-γ、IL-6均显著优于对照组(P 0. 05)。结论恩替卡韦联合聚乙二醇干扰素治疗CHB患者疗效良好,可有效抑制乙型肝炎病毒复制,协同发挥抗病毒作用,安全性高。     

阿德福韦联合拉米夫定与恩替卡韦治疗耐药性慢性乙肝疗效比较

目的对于拉米夫定耐药慢性乙肝患者采用阿德福韦联合拉米夫定用药,与单用恩替卡韦治疗比较临床效果与不良反应。方法将耐药慢性乙肝患者42例随机分为两组：阿德福韦联合拉米夫定治疗组（联合用药组）22例．恩替卡韦治疗组（对照组）20例,疗程均为48周,观察两组患者肝功能、HBV-DNA等相关指标。结果（1）治疗24周后,血清ALT复常率、HBV-DNA转阴率、HBeAg转阴率、HBeAg转换率4项指标两组比较,联合组分别为72．7％、68．2％、31．8％、9．0％,对照组分别为75．0％、70．0％、30．0％、10．0％。（2）治疗48周后,血清ALT复常率、HBV-DNA转阴率、HBeAg转阴率、HBeAg转换率4项指标两组比较,联合组分别为86．3％、81．8％、72．7％、36．3％。对照组分别为85．0％、80．0％、75．0％、30．0％。（3）治疗48周后．对照组发生变异4例（20．0％）．联合组病毒变异无1例发生。两组病毒变异率比较差异有统计学意义（P〈0．05）。结论阿德福韦联合拉米夫定治疗拉米夫定耐药的慢性乙肝的I临床疗效与安全性与恩替卡韦相似,但病毒耐药变异率较恩替卡韦低。     

核苷类抗病毒药物治疗失代偿期乙型肝炎肝硬化的临床效果观察

目的观察核苷类药物治疗乙型肝炎肝硬化失代偿期的效果。方法204例乙型肝炎肝硬化失代偿期患者随机分为4组,所有患者在保肝对症治疗的基础上,分别给子拉米夫定（A组）100mg／d,阿德福韦酯（B组）10mg／d,恩替卡韦（C组）0．5mg／d,13服,疗程为48周。同时设立保守治疗组（D组）,仅用一般保肝药物如复方益肝灵等。观察所有患者临床症状、体征、肝功能变化、凝血酶原时间活动度（PTA）,HBV-DNA定量、HBeAg阴转、HBeAg／HBeAb转换情祝。结果通过抗病毒治疗,肝功能、PTA均有明显改善。HBeAg血清转换率A、B、C组分别为31．4％（16／51）、27．5％（14／51）、37．3％（19／50）,3组比较差异有统计学意义（P〈0．05）,HBV—DNA阴转率A、B、C组分别为84．3％（43／51）、62．0％（31／50）、90．2％（46／51）,组间比较差异有统计学意义（P〈0．05）。B组死亡1例,D组效果最差,死亡4例。抗病毒治疗组与保守治疗组疗效差异有统计学意义（P〈0．01）。结论乙型肝炎肝硬化失代偿期患者应行抗病毒治疗,可首先选用恩替卡韦或拉米夫定,为防止应用拉米夫定病毒变异,可在病情好转后改用阿德福韦酯继续治疗。     

4种抗病毒方案治疗慢性乙型肝炎的疗效分析

目的：观察4种抗病毒方案治疗慢性乙型肝炎（CHB）的疗效。方法将240例CHB患者按用药情况分为A、B、C、D组,分别给予口服拉米夫定、阿德福韦酯、阿德福韦酯/拉米夫定、恩替卡韦。比较各组治疗12、24、48周时的丙氨酸氨基转移酶（ALT）、天门冬氨酸氨基转移酶（AST）复常率,HBVDNA水平及转阴率,HBeAg/HBeAb转换率以及治疗48周时的YMDD变异率。结果C组和D组的ALT、AST复常率,HBVDNA水平及转阴率,HBeAg/HBeAb转换率,以及YMDD变异率均优于A组和B组,差异均有统计学意义（P＜0．05）。结论阿德福韦酯/拉米夫定和恩替卡韦是2种合理的治疗方案。     

HBV基因型及其临床意义的研究

目的：探讨乙型肝炎病毒基因型与临床表现及干扰素联合猪苓多糖抗病毒治疗后HBV DNA、HBeAg的关系。方法；研究病例39例，入选病例32例，采用微板核酸杂交ELISA法进行基因分型，干扰素a-2b500万u，每周3次，疗程6个月；同时给予猪苓多糖4mL，1次／d，疗程2个月。观察HBV DNA、HBeAg、HBeAg／抗-HBe的变化。结果；32例样本中，B型，C型，B、C混合型分别为37．5％、50％、12．5％，发现家族中连续二代基因型的变化，同时发现联合抗病毒治疗的疗效并未在基因亚型中产生差异。结论：慢性HBV感染者不同类型肝病中基因型B和基因型C所占比例有差异。从家族中连续二代基因型的变化可以看出。基因分型又是相对的，基因亚型间存在自然的变异。     

恩替卡韦初治HBeAg阳性的慢性乙型肝炎肝纤维化疗效评价

目的评价恩替卡韦和阿德福韦酯抗慢性乙型肝炎肝纤维化的效果。方法选择2007年10月至2009年10月HBeAg阳性的慢性乙型肝炎患者158例予恩替卡韦抗病毒治疗,另选择同期的HBeAg阳性慢性乙型肝炎患者167例予阿德福韦酯抗病毒治疗,观察2组患者治疗前、治疗后12、24个月乙型肝炎病毒(HBV)-DNA阴转率、HBeAg阴转率及血清肝纤维化指标的变化情况。随机对其中42例恩替卡韦治疗者、36例阿德福韦酯治疗者治疗前和治疗后24个月行肝组织穿刺术作组织炎症活动度和纤维化程度的评分比较。结果恩替卡韦组患者治疗12、24个月HBV-DNA阴转率分别为68.4%、80.4%,明显高于阿德福韦酯组患者的31.1%、41.9%(P均<0.05);2组HBeAg阴转率比较差异无统计学意义(P>0.05)。2组患者治疗后血清肝纤维化指标(PCⅢ、LN、HA、ⅣC)水平均低于治疗前(P均<0.01),且恩替卡韦组治疗后各指标均低于阿德福韦酯组(P均<0.05)。恩替卡韦组治疗后24个月组织学炎症活动度、肝纤维化程度评分均低于阿德福韦酯组,差异均有统计学意义(P<0.05)。结论肝纤维化程度的改善与抗病毒疗效密切相关,恩替卡韦治疗HBeAg阳性的慢性乙型肝炎较阿德福韦酯更能抑制HBV复制,可改善肝纤维化程度。     

Hepatitis B virus genotypes and response to antiviral therapy

Hepatitis B virus (HBV) infection is an important health problem worldwide. The virus has been classified according to 8 genotypes (A-H) based on sequence divergence. Most genotypes have specific geographic distributions; genotypes A and D are prevalent in Western Europe and North America, and genotypes B and C are prevalent in East Asia and Oceania. Currently accepted treatment for chronic hepatitis B includes interferon alpha, or the nucleoside/nucleotide analogues lamivudine and adefovir. The impact of HBV genotypes on response to antiviral therapy has been studied. HBV genotypes D and C are associated with a lower rate of favorable response to interferon alpha therapy than genotypes A and B, respectively. A study in Germany suggested that the rate of resistance to lamivudine was higher in patients with HBV genotype A infection than in patients with genotype D infection. No difference in the risk of lamivudine resistance is found between patients with genotype B and patients with genotype C. In patients with genotype C infection, however, virological response is worse during lamivudine therapy, and is also less durable after the discontinuation of therapy than in patients with genotype B infection. Determining the genotype could be helpful for predicting the outcome of antiviral therapy in patients with chronic hepatitis B.     

Hepatitis B genotypes and response to antiviral therapy: a review

The aim of this review is to examine the impact of hepatitis B virus (HBV) genotypes on biochemical and virologic response to antiviral drugs (alfa-interferon and pegylated-interferon alfa-2b, lamivudine, and adefovir dipivoxil) actually used for the treatment of chronic hepatitis, HBV related. International literature evidences that HBV genotypes D and C are associated with a lower rate of favorable response to alfa-interferon and pegylated-interferon alfa-2b therapy than genotypes A and B. The rate of resistance to lamivudine was higher in patients with genotype A infection than in patients infected by genotype D, whereas no difference in the risk of lamivudine resistance is found between patients with genotype B and patients with genotype C. In regard to the new nucleotide analogue, adefovir dipivoxil, a preliminary trial appears to provide no evidence of any difference in virologic response among the different HBV genotypes. The current study has determined that the different HBV genotypes have a very important impact on response to antiviral therapy, in particular interferon treatment. For this reason, determining the HBV genotype could be helpful for predicting the outcome of antiviral therapy in patients affected by chronic hepatitis B.     

Hepatitis B virus genotype-associated variability in antiviral response to adefovir dipivoxil therapy in Chinese Han population

It is well known that different genotypes of hepatitis B virus (HBV) have a different sensitivity to interferon-alpha or lamivudine (nucleoside analogue) antiviral therapy. However, for adefovir dipivoxil (ADV, a nucleotide analogue), the antiviral response of the different genotypes remains to be clarified. In order to evaluate the response of HBV genotypes to ADV therapy and to identify factors that might affect initial virological response, we performed a retrospective analysis on patients with chronic hepatitis B (CHB) in Chinese Han population. The study included 183 patients, who had been tested positive for hepatitis B e antigen (HBeAg) and had been treated with ADV (10 mg/day) for 48 weeks. The numbers of patients infected with HBV genotype B and genotype C were 98 and 75 cases, respectively, and the remaining 10 patients were mixture infection of genotypes B plus C or genotypes B plus D. The mean HBV-DNA reduction and HBV-DNA seroclearance of genotypes B and C at 48 weeks were 3.6 log(10) and 3.1 log(10) copies/ml (p < 0.05) and 41.8% and 34.6% (p < 0.05), respectively. There were no statistically significant differences between genotypes B and C in terms of HBeAg loss, anti-HBe seroconversion and normalization of serum alanine aminotransferase (ALT). Multivariate analysis showed that young age, low pretreatment HBV-DNA and/or elevated ALT level might be independent predictive factors associated with initial virological response. Thus, in Han CHB patients who are HBeAg-positive, HBV genotype B shows a better virological response to ADV therapy than does genotype C.     

Hepatitis B virus genotypes B and C do not affect the antiviral response to lamivudine

To date, there have been no studies examining the role of hepatitis B virus (HBV) genotypes on the response to lamivudine therapy and the development of YMDD mutations. The present study aimed at determining any differences in the antiviral response and risk of YMDD mutations between lamivudine-treated patients with HBV genotype B and genotype C. Eighty-two patients receiving lamivudine were recruited. HBV genotypes at baseline and YMDD mutations at week 52 were determined by line probe assays (LiPA). HBV DNA levels were determined by the Cobas Amplicor HBV Monitor Test. Seventeen (20.7%) and sixty-four (78%) patients had single genotypes of B and C, respectively. At both week 24 and 52 there were no differences in the median reduction of HBV DNA levels (median 4 logs drop), the median reduction of alanine aminotransferase (ALT) levels, and the proportion with normalization of ALT [8/8 (100%) vs 26/37 (70.3%), P=0.19] between patients with genotypes B and C. The rate of HBeAg seroconversion [3/17 (17.6%) vs 6/64 (9.4%), P=0.39] and the chance of YMDD mutation development [3/17 (17.6%) vs 12/64 (18.8%), P=1.0] at week 52 were also similar between patients with genotype B and C, respectively. In conclusion, there was no difference in the antiviral response and the rate of development of YMDD mutations in Chinese patients with genotype B and C after 1 year of lamivudine. Determination of HBV genotypes before lamivudine therapy was probably not an important pretreatment investigation to predict antiviral responses in Chinese patients.     

江苏地区乙型肝炎患者HBV基因分型与血清HBV DNA水平研究

目的了解江苏地区乙型肝炎病毒基因型分布特征,探讨HBV各基因型与血清HBV DNA水平、患者年龄之间的关系。方法采用荧光定量PCR结合Taqman MGB探针技术,对江苏地区176份乙型肝炎患者血清中的HBV DNA进行基因分型和定量检测。结果176例血清中,C型117人(66.5%),B、C型40人(22.7%),B型9人(5.1%),D型1人(0.6%),A型1人(0.6%)。C型与B、C混合型在HBV DNA水平上存在显著差异(t=2.413,P<0.05),B、C混合型的HBV DNA水平明显高于C型。C基因型在慢性乙型肝炎患者中的所占比例(71.4%)比在急性乙型肝炎、肝硬化和肝癌患者中所占的比例较高,但差异无显著性。HBV DNA各基因型在患者年龄水平上没有明显差异(P>0.05)。结论江苏地区HBV基因型以C型为主、B、C混合型次之,B型较少,D型、A型极少;B、C混合型患者的HBV DNA数量水平显著高于C型。     

Hepatitis B virus genotypes and hepatocellular carcinoma in Taiwan

With phylogenetic analysis of hepatitis B virus (HBV) isolates, eight different genotypes (A to H) have been recognized worldwide. The impact of HBV genotypes on the clinical aspects of HBV infection in Taiwan, including the clinical outcome of chronic infection and therapeutic response to antiviral treatments, has been clarified. Our data showed that genotypes B and C are the predominant HBV strains in Taiwan, and genotype C is associated with more severe liver disease including cirrhosis and hepatocellular carcinoma (HCC), whereas genotype B is associated with the development of HCC in young noncirrhotic patients. Serologically, genotype C tends to have a higher frequency of hepatitis B e antigen (HBeAg) positivity and a higher serum HBV DNA level than genotype B. In addition, genotype C patients, compared to genotype B patients, have a delayed HBeAg seroconversion in the immune clearance phase of chronic HBV infection. Virologically, genotype C bears a higher frequency of basal core promoter mutation than genotype B. Our recent data further indicated that patients with basal core promoter mutation are significantly more associated with the development of HCC than those without, which applies to both genotypes B and C. In addition, the prevalence of basal core promoter mutation in young HCC patients is comparable to older HCC patients but is significantly higher than that in age-matched inactive carriers, irrespective of genotypes. Although superinfection of HBV on hepatitis B carriers indeed occurs in Taiwan, it is rarely associated with acute exacerbations. As to the response to antiviral treatments, genotype C is associated with a lower response rate to interferon therapy compared to genotype B. In addition, genotype B seems to have a better virological response to lamivudine as compared to genotype C, but both genotypes have a similar risk in the development of lamivudine resistance. These lines of evidence highlight the remarkable differences in the clinical and virological characteristics between Taiwanese patients infected with different genotypes. In conclusion, pathogenic and therapeutic differences do exist among HBV genotypes in Taiwan, and determining the genotype in patients with chronic HBV infection would help gain further information in anthropologic, clinical, virological and prognostic investigations.     

慢性乙型肝炎基因分型与阿德福韦酯疗效相关性研究

目的 调查本地区乙型肝炎病毒(HBV)基因分型的分布情况,观察乙型肝炎基因分型对阿德福韦酯抗病毒疗效的影响.方法 对285例慢性乙型肝炎(其中HBV基因型B型219例,C型66例)用阿德福韦酯治疗的慢性乙型肝炎的患者进行分析,观察治疗12周、24周、48周及96周丙氨酸转氨酶(ALT)、HBV DNA定量、乙型肝炎病毒e抗原(HBeAg)乙型肝炎病毒e抗体定量.结果 阿德福韦酯治疗12周时B组以及C组HBV DNA转阴率为30.6%及36.4%,HBV DNA下降均值为(1.36±0.98)eopies/ml及(1.31±1.40)copies/ml(P>0.05);治疗24周两组HBV DNA转阴率分别为33.8%及42.4%,HBV DNA下降均值为(2.19±1.18)copies/ml及(2.22±1.10)copies/ml(P>0.05).治疗48周两组HBV DNA转阴率分别为38.8%及45.5%,HBV DNA下降均值为(2.98±1.24)copies/ml及(2.97±0.92)copies/ml(P>0.05).治疗96周两组HBV DNA转阴率分别为44.8%及48.5%,HBV DNA下降均值为(3.41±1.68)copies/ml及(3.50±1.72)copies/ml(P>0.05).治疗12周后B、C两组HBeAg转阴HBeAb出现分别为10.6%vs 8.6%及11.6%vs 9.3%,24周后B、C两组HBeAg转阴/HBeAb出现分别为14.6%vs 11.3%及16.3%vs 11.6%,48周后B、C两组HBeAg转阴/HBeAb出现分别为27.8%vs 21.2%及25.6%vs 20.9%,96周后B、C两组HBeAg转阴/HBeAb出现分剐为36.4%vs 25.2%及39.5%vs 25.6%,两组差异均无统计学意义(P>0.05).两组ALT复常率12周为59.8%vs 47.0%(P<0.05),24周为60.3%vs 63.6%,48周为76.3%vs 77.3%,96周为80.0%vs 80.3%,两组差异均无统计学意义(P>0.05).结论 阿德福韦酯治疗慢性乙型肝炎B型及C型,病毒应答、生化应答及血清学应答相当,阿德福韦酯时HBV基因B型及C型疗效无明显影响.本地区HBV基因型以B型为主,C型次之,未发现A、D型.     

Genetic variability of hepatitis B virus and response to antiviral therapy

Hepatitis B virus (HBV) infection is a global health issue. Effective and individualized treatment of chronic hepatitis B to prevent progression to end-stage liver diseases and hepatocellular carcinoma is needed. HBV can be classified into eight genotypes (A-H) on the basis of genome sequence divergence. In addition, several naturally occurring HBV mutants have also been identified. The epidemiology of HBV genotypes and their implications for response to antiviral therapy have become increasingly recognized. Recent studies suggested that responses to standard interferon treatment in patients with genotype A or B are better than those with genotype C or D; however, conflicting results exist regarding the response to pegylated interferon. The influence of dose and duration on interferon-based therapy remains to be clarified. In addition to genotype, naturally occurring mutations such as precore and core promoter mutations have also attracted much attention, because they have been shown to affect the disease progression of HBV-related chronic liver disease and possibly the response to antiviral therapy. Here, we review the differences in antiviral theraputic response among HBV genotypes and discuss the role of precore or core promoter mutations in response to antiviral therapy.     

湘潭地区乙型肝炎病毒基因型与YMDD基因区序列突变及BCP区突变关系探讨

【目的】对湘潭地区HBV感染者的基因型、YMDD基因区序列突变及BCP区突变情况及关系进行探讨。【方法】对952例不同类型的HBV感染者的样本同时进行基因型、YMDD基因区序列突变及BCP区突变检测和分析。【结果】湘潭地区HBV各种基因型分布比例为：B型占73．32％,C型占12．08％,B、C型混合感染14．60％。YMDD基因区序列突变结果显示：YMDD野生型,占88．66％,其余为YMDD突变型。BCP区突变结果显示：1762A／1764G（野生型）占70．59％,1762T／1764A（突变型）占19．75％,其余为混合型。基因型、相关性分析显示：HBVB型和C型YMDD基因区序列突变率无显著性差异（P〉0．05）,序列突变类别存在显著性差异（P〈0．05）,HBVC型YVDD突变率要高于B型。C型BCP区突变率要高于B型（P〈0．01）。HBV YMDD野生型和突变型的BCP区突变率存在显著性差异（P〈0．01）,HBV YMDD突变型标本BCP区突变率与YMDD野生型相比无差异,但YVDDBCP区突变率要高于其他类别。【结论】①湘潭地区流行的HBV基因型主要为B型和C型,其中B型为优势基因型,具有南方地区的特点。②拉米夫定治疗前通过HBV基因型检测来预测抗病毒应答可能并无实际意义。③HBV基因分型、YMDD基因区序列突变、BCP区突变检测的应用,将有助于临床上对乙肝患者的预后和转归进行正确评价。     

乙肝病毒基因变异和基因型(亚型)与肝细胞癌的关系

目的 初步探讨乙肝病毒基因变异、基因型及亚型与HCC发病的相关性。 方法 特异探针杂交法检测乙肝病毒C启动子变异，分别用特异探针杂交和特异引物PCR两种方法鉴定病毒基因型，限制性酶切片段长度多态性法鉴定部分HCC乙肝病毒的基因亚型。用SPSS10.0进行统计分析其中相关性。 结果 HCC组与NHCC组HBV-DNA载量无显著差异，两组HBV中A1762T/G1764A变异株分别占77.8%和44.4%。B和C型为HBV主要基因型，基因型B和C在HCC患者中分别为3例（11.11%）和24例（88.89%），在NHCC患者中分别为29例（42.65％）和21（50.85％），HCC组24例基因型C的HBV中21例为C2亚型。 结论 乙肝病毒C启动子A1762T/G1764A双变异、基因型C与HCC的发生密切相关，HCC患者HBV基因亚型主要为C2亚型。