《2022医学课件传染病Viral-hepatitis》由会员分享，可在线阅读，更多相关《2022医学课件传染病Viral-hepatitis（94页珍藏版）》请在金锄头文库上搜索。
1、1Viral hepatitisTianjin Medical University General HospitalDepartment of Infectious Diseases逄崇杰逄崇杰第一页，共九十四页。2难点难点nHBV形态、基因组结构和编码蛋白nHBV、HCV的发病机制n肝炎的临床分类和临床表现慢肝和重肝nHBV抗原-抗体系统的组成和意义n慢性HBV、HCV的治疗nHBV的母婴阻断第二页，共九十四页。3重点和问题重点和问题n定义：病毒性肝炎，定义：病毒性肝炎，Dane颗粒，慢性肝炎，窗口期，颗粒，慢性肝炎，窗口期，cccDNA，胆，胆酶别离酶别离nHBV在人体内的复制过程和发病
2、机制在人体内的复制过程和发病机制nHCV感染易转为慢性的原因感染易转为慢性的原因nHBV抗原抗原-抗体系统的组成和意义抗体系统的组成和意义n各型病毒性肝炎的传播途径各型病毒性肝炎的传播途径n病毒性肝炎的临床分类病毒性肝炎的临床分类n重型肝炎的并发症重型肝炎的并发症n慢性乙肝、丙肝的药物治疗慢性乙肝、丙肝的药物治疗n意外暴露意外暴露HBV后的预防后的预防第三页，共九十四页。4IntroductionnViral hepatitis is a group systemic communicable disease affecting the liver predominantly caused b
3、y some kinds of virusesnViral hepatitis may be divided into 5 types according to etiology, that is hepatitis A, B, C, D and EnAlthough the agents can be distinguished by its antigenic properties, the 5 kinds of viruses may produce clinical similar illness第四页，共九十四页。5IntroductionnClinical manifestatio
4、ns are characterized by anorexia, nausea, fatigue, enlarged liver and abnormal liver function, a part of cases may appear jaundice. nHepatitis A and E shows acute hepatitis, fecal-oral route predominantlynHepatitis B, C and D predispose to a chronic hepatitis and is related to liver cirrhosis and he
5、patic cancer, humoral transmission. 第五页，共九十四页。6IntroductionnRecently, 3 kinds of viruses named GBV-C, TTV and SENV are discovered, and not yet considered to relate to viral hepatitis第六页，共九十四页。7Etiology: Hepatitis A virus (HAV)nHAV is one kind of picornavirus微小RNA病毒科 and used to be classified as ente
6、rovirus type 72, but recently, it is considered to be classified as heparnavirus嗜肝RNA病毒属nHepatitis A virion is a spherical particle, diameter 2732nmnConsists of a genome of linear, single-stranded RNA, 7.5kb第七页，共九十四页。8Etiology: Hepatitis A virus (HAV)nSeven gene types, 1, 2, 3, 4 types from human bo
7、dynOnly one antigen-antibody system. Anti-HAV IgM is diagnostic evidence of recent infection, IgG is protective antibody.nDuring acute stage of infection, HAV can be found in blood and feces of infected human第八页，共九十四页。9Etiology: Hepatitis B virus (HBV)nA kind of hepadnavirus嗜肝DNA病毒科n19651967, Blumbe
8、rg and Krugman, hepatitis associated antigen, HAAn1972, hepatitis B surface antigen, HBsAgn1970, Dane particlen1979, genomewide sequence finished 第九页，共九十四页。10Baruch S. Blumberg July 28, 1925April 5, 2022After receiving the prize, he was invited to China. “I spoke before several thousand people, he t
9、old The Times in 2002. “I provided them with a copy of the patent, and now Im told that it helped to change the direction of what they were doing and led to the saving of a lot of lives. “Saving lives, he said, “is the whole point of his career, and “This is what drew me to medicine. There is, in Je
10、wish thought, this idea that if you save a single life, you save the whole world, and that affected me. Nobel Prize in Physiology or Medicine in 1976 第十页，共九十四页。11Etiology: Hepatitis B virus (HBV)nThree particles in serum nSpherical particles with a diameter of 22nm and tubular particles, composed of
11、 HBsAgnLarge particles with a diameter of 42 nm, named Dane particle. It is a complete infectious HBV particles, consists of an outer protein shell (envelope, contain HBsAg) and an inner body ( core, contain HBcAg, HBeAg, HBV-DNA and DNAP )第十一页，共九十四页。12large particlesspherical particlestubular parti
12、cles第十二页，共九十四页。13Etiology: Hepatitis B virus (HBV)nHepatitis B virion genome is a small circular, partially double stranded DNA with 3.2kb. nHBV DNA is asymmetry in length of two strands: minus strand (long strand, L) has full length. 第十三页，共九十四页。14第十四页，共九十四页。15Etiology: Hepatitis B virus (HBV)nFour
13、open reading frames (ORF) nS region: include pre-s1, pre-s2 and S gene, encoded pre-s1 protein, pre-s2 protein and S proteinnC region: included pre-c and C gene, encode HBeAg and HBcAgnP region: encoded DNA polymerasenX region: encoded HBxAg第十五页，共九十四页。16Etiology: Hepatitis B virus (HBV)nThree antige
14、n-antibody systemnHBsAganti-HBsnHBeAganti-HBenHBcAganti-HBcnpre-s1, pre-s2anti-pre-s1, anti-pre-s2 第十六页，共九十四页。17Etiology: Hepatitis B virus (HBV)nHBsAg：疾病早期出现，一般在ALT升高前16w，急性者持续5w5m，慢性者可持续多年n抗HBs： HBsAg消失后数周出现，可保持多年n前S1，前S2抗原：紧随HBsAg出现在血液中，与HBV活泼复制有关，也可作为评价药物疗效的指标n前S1抗体：潜伏期出现n前S2抗体：出现于HBV复制终止前后，提示HB
15、V去除第十七页，共九十四页。18Etiology: Hepatitis B virus (HBV)nHBcAg：肝细胞坏死后释放入血，易与核心抗体形成抗原肝细胞坏死后释放入血，易与核心抗体形成抗原抗体复合物而不易检出抗体复合物而不易检出n抗抗HBc IgM：存在与乙肝急性期及慢乙肝急性发作期，存在与乙肝急性期及慢乙肝急性发作期， HBsAg阳性后阳性后24周出现周出现n抗抗HBc IgG：抗抗HBc IgM下降消失后出现，可持续多年，下降消失后出现，可持续多年，为为HBV既往感染的标志既往感染的标志n窗口期：窗口期：HBV感染时，感染时，HBsAg已消失，抗已消失，抗HBs尚未出现，血尚未出现
16、，血中仅能检出抗中仅能检出抗HBc/抗抗HBe，此期可能有传染性，此期可能有传染性第十八页，共九十四页。19Etiology: Hepatitis B virus (HBV)nHBeAg：仅见于HBsAg阳性血清，稍后或同时于HBsAg在血中出现，HBV复制和传染性强的标志n抗抗HBe：紧随HBeAg消失而出现，表示HBV复制减少和传染性减低n前前C区变异：区变异：HBeAg阴性nHBV-DNA：位于HBV核心，与HBeAg同时出现于血中，是HBV感染最直接，特异，灵敏的指标。分为游离型及整合型nHBVDNAP：位于HBV核心，具有逆转录酶特性，是直接反映HBV复制能力的指标第十九页，共九十四页。20乙型肝炎病毒急性感染模式乙型肝炎病毒急性感染模式1010周周周周2020周周周周3030周周周周2 4 6 8 102 4 6 8 10 年年年年感染感染感染感染HBVHBV后时间后时间后时间后时间第二十页，共九十四页。21Etiology: Hepatitis C virus (HCV)nHCV is a member of flaviviridae黄病毒科 nHCV genome is
