乙型肝炎慢性化机制的研究现状

纪翠霞; 胡九东; 邢练军; 季光; 王磊

乙型肝炎慢性化机制的研究现状

1. 上海中医药大学附属龙华医院肝病科
2. 上海中医药大学脾胃病研究所

详细信息

中图分类号: R512.62
计量
- 文章访问数: 3274
- HTML全文浏览量: 22
- PDF下载量: 818
- 被引次数: 0
出版历程
- 出版日期: 2012-02-20

Research on pathogenetic mechanism of chronic hepatitis B

摘要

摘要: 感染HBV后出现不同的结局:(1)急性自限性肝炎;(2)慢性肝炎;(3)慢性HBV携带者或HBsAg携带者;(4)隐匿性慢性乙型肝炎;(5)乙型肝炎肝硬化;(6)重型肝炎。除急性自限性肝炎和重型肝炎外,其余四种都可以成为慢性HBV感染。慢性乙型肝炎是一个慢性过程,肝硬化、肝细胞癌与之呈正相关。因此,治愈乙型肝炎、预防肝硬化与肝癌的发生是我们研究的重点和努力的方向。要解决乙型肝炎这个问题,必须了解乙型肝炎慢性化的形成机制。近些年,对乙型肝炎慢性化的形成机制有了不少新的研究成果,其中主要与病毒载量、基因型和宿主免疫状态等有关,作者查找了近年有关这方面的研究,现作一综述。
- 肝炎,乙型,慢性 /
- 肝炎病毒,乙型 /
- 病毒载量 /
- 基因型 /
- 免疫力
Abstract: There will be some different outcomes after HBV infection: (1) acute self-limited hepatitis B; (2) chronic hepatitis; (3) chronic HBV carriers or HBsAg carriers; (4) occult chronic hepatitis B; (5) cirrhosis caused by chronic hepatitis B; (6) severe hepatitis.And (2) (3) (4) (5) could be called chronic HBV infection.Chronic hepatitis B is a long process which is positively correlated with cirrhosis and hepatocellular carcinoma.It is very important to cure chronic hepatitis B and prevent the occurrence of cirrhosis and hepatocellular carcinoma.Recently, lots of research achievements on the pathogenetic mechanism of chronic hepatitis B were reported, which mainly were related to viral load, genotype and state of the host immune.This article summarizes recent developments on pathogenetic mechanism of chronic hepatitis B.
- hepatitis B /
- chronic /
- hepatitis B virus /
- viral load /
- genotype

HTML全文

参考文献(28)

[1] 中华医学会.慢性乙型肝炎防治指南[J].肝脏, 2011, 16 (1) :2-5.

[2]Asabe, S, Wieland SF, Chattopadhyay PK, et al.The size ofthe viral inoculum contributes to the outcome of hepatitis Bvirus infection[J].J Virol, 2009, 83 (19) :9652-9662.

[3]孙颖, 滕光菊, 邹正升, 等.37例急性乙型肝炎患者临床和病毒学变化特征分析[J].实用肝脏杂志, 2011, 14 (1) :21-22.

[4]周建.慢性乙型肝炎患者HBV-DNA载量、IL-10水平与肝损伤的相关性[J].实验与检验医学, 2010, 28 (6) :591-592.

[5]Goulder PJ, Watkins DI.Impact of MHC class I diversity onimmune control of immunodeficiency virus replication[J].Nat Rev Immunol, 2008, 8 (8) :619-630.

[6]陈冬梅, 高冀荣, 都特, 等.HLA-DQA1基因多态性与HBV感染结局相关[J].基础医学与临床, 2006, 26 (5) :494-497.

[7]骆峻, 金安娜, 吴旭东, 等.中国人群HLA-DRB1基因多态性与慢性乙型肝炎关系的Meta分析[J].世界华人消化杂志, 2006, 14 (31) :3050-3054.

[8] 卢志明.杀伤细胞免疫球蛋白样受体基因多态性与HBV感染和转归的关联研究[D].济南:山东大学, 1983:1-103.

[9]Awan Z, Idrees M, Amin I, et al.Pattern and molecular epi-demiology of hepatitis B virus genotypes circulating in Paki-stan[J].Infect Genet Evol, 2010, 10 (8) :1242-1246.

[10]Eksteen B, Afford S C, Wigmore S J, et al.Immune-media-ted liver injury[J].Semin Liver Dis, 2007, 27 (4) :351-366.

[11]Gao B, Jeong WI, Tian Z.Liver:an organ with predominantinnate immunity[J].Hepatology, 2008, 47 (2) :729-736.

[12]韩亚萍, 刘源, 李军, 等.肝病患者的肝组织单细胞悬液与外周血中淋巴细胞亚群的分析比较[J].检验医学, 2005, 20:448-451.

[13]Kaneko Y, Harada M, Kawano T, et al.Augmentation of Val-pha 14NKT cell-mediated cytotoxicity by interleukin 4 in anautocrine mechanism resulting in the development of con-canavalin A-induced hepatitis[J].Exp Med, 2000, 191 (1) :105-114.

[14]欧强, 陈良, 孙洪清, 等.慢性HBV感染者外周血T淋巴细胞亚群和NK细胞活性变化[J].临床肝胆病杂志, 2006, 22 (4) :277-278.

[15]Emoto M, Kaufmann SH.Liver NKT cells:an account of heter-ogeneity[J].Trends in immunol, 2003, 24 (7) :364-369.

[16]Velázquez P, Cameron TO, Kinjo Y, et al.Cutting edge acti-vation by innate cytokines or killer t cell patrolling of liver sinu-soids[J].J Immunol, 2008, 180 (4) :2024-2028.

[17]Li J, Han Y, Wan Y, et al.Dynamic changes of cytotoxic Tlymphocytes (CTLs) , natural killer (NK) cells, and naturalkiller T (NKT) cells in patients with acute hepatitis B infec-tion[J].Virol J, 2011, 8:199.

[18]黄芳.慢性乙型肝炎T淋巴细胞活化与免疫耐受相关性的初步研究[D].长沙:中南大学, 2007:1-41.

[19]Woltman AM, Op den Brouw ML, Biesta PJ, et al.Hepatitis Bvirus lacks immune activating capacity, but actively inhibits plas-macytoid dendritic cell function[J].PloS One, 2011, 6 (1) :15324.

[20]Akbar SM, Horiike N, Chen S, et al.Mechanism of restora-tion of immune responses of patients with chronic hepatitis Bduring lamivudine therapy:increased antigen processing andpresentation by dendritic cells[J].J Viral Hepat, 2011, 18 (3) :200-205.

[21]张蓓.CD4+CD25+调节性T细胞在慢性持续性乙型肝炎病毒感染中的作用临床研究[D].重庆:第三军医大学, 2007:1-91.

[22]肖光明, 姚细安, 连粤湘, 等.乙型肝炎患者外周学T淋巴细胞亚群的变化[J].实用肝脏杂志, 2005, 8:22-24.

[23]Thimme R, Wieland S, Steiger C, et al.CD8 (+) T cells medi-ate viral clearance and disease pathogenesis during acute hepa-titisB virus infection[J].J Virol, 2003, 77 (1) :68-76.

[24]Bertoletti A, Ferrari C.Kinetics of the immune response duringHBV and HCV infection[J].Hepatology, 2003, 38 (1) :4-13.

[25]赵英仁, 郑婕, 张树林.慢性乙型肝炎Th1/Th2失衡分析[J].第四军医大学学报.2004, 25 (5) :468-470.

[26]Jing XH, Sun YN, Huang ZQ, et al.Effect of interferon onlevels of cytokines and on result of anti-virus in patientswith chronic hepatitis B[J].China Journal of Modern Medi-cine, 2004, 14 (24) :76-78.

[27]福军亮, 徐东平, 施明, 等.乙型肝炎患者外周血CIMCD25调节性T细胞型与功能分析[J].中华内科杂志, 2006, 45 (8) :642-645.

[28]张慧, 黄丽霞, 陈朝霞, 等.CD4+CD25+Foxp3+Treg细胞在HBV感染所致慢加急性肝衰竭中作用[J].东南大学学报 (医学版) , 2011, 30 (2) :315-318.

施引文献

资源附件(0)

访问统计