人類免疫缺陷病毒 (HIV) 是人獲得性免疫缺陷綜合征 (愛滋病，AIDS) 的致病原，2010年全球有180萬人死於愛滋病，HIV/AIDS已成為全球健康的嚴重挑戰。人類免疫缺陷病毒與乙型肝炎病毒 (HBV) ，丙型肝炎病毒 (HCV) 的合併感染非常普遍，已演變成具有嚴重臨床後果的新健康問題。儘管對於人類免疫缺陷病毒的研究已有很大的進展，但由於受研究模型的限制，人體免疫系統對人類免疫缺陷病毒感染的應答，特別是對乙型肝炎病毒，丙型肝炎病毒與人類免疫缺陷病毒合併感染的免疫應答，仍值得進一步的闡明。 / 在本研究中，我們首先對深圳人類免疫缺陷病毒，乙型肝炎病毒，丙型肝炎病毒合併感染的流行情況進行研究。共選取914份人類免疫缺陷病毒感染者的血漿，經過對乙型肝炎病毒表面抗原 (HBsAg) 和抗丙型肝炎病毒抗體 (anti-HCV) 的檢測，發現10.9% (100/914) 的被檢測者是人類免疫缺陷病毒/乙型肝炎病毒合併感染，14.6% (133/914) 為人類免疫缺陷病毒/丙型肝炎病毒合併感染，3.7% (34/914) 為人類免疫缺陷病毒/乙型肝炎病毒/丙型肝炎病毒三重感染。多元邏輯回歸分析證明人類免疫缺陷病毒傳染的危險行為與合併感染顯著相關聯。大多數的人類免疫缺陷病毒/乙型肝炎病毒合併感染者都是通過性接觸感染人類免疫缺陷病毒，包括異性傳播與同性傳播 (95/100, 95%); 大多數的人類免疫缺陷病毒/丙型肝炎病毒合併感染者是靜脈注射吸毒者 (89/133, 66.9%); 人類免疫缺陷病毒/乙型肝炎病毒/丙型肝炎病毒三重感染者中，大多數是靜脈注射吸毒者 (28/34, 82.4%)。靜脈注射吸毒人群中，大部分是男性 (108/122, 88.5%)，約半數人的年齡介乎27至32歲 (56/122, 45.9%) 。有接近一半的經過血液和血液製品傳播人類免疫缺陷病毒的人是人類免疫缺陷病毒/丙型肝炎病毒合併感染者 (10/23, 43.5%) 。性別與人類免疫缺陷病毒感染的危險行為有顯著關係，大部份的靜脈注射吸毒者是男性。 / 進一步，我們利用酶聯免疫吸附測定法 (ELISA) 檢測深圳愛滋病陽性樣本血漿中白細胞介素27 (IL-27) 的濃度。結果顯示，對比健康參照者，人類免疫缺陷病毒單獨感染者，人類免疫缺陷病毒/乙型肝炎病毒合併感染者，人類免疫缺陷病毒/丙型肝炎病毒合併感染者的血漿IL-27濃度顯著升高。隨後我們進一步發現，人類免疫缺陷病毒單獨感染組，人類免疫缺陷病毒/乙型肝炎病毒，人類免疫缺陷病毒/乙型肝炎病毒/丙型肝炎病毒合併感染組之間的血漿IL-27濃度沒有顯著差異，而人類免疫缺陷病毒/丙型肝炎病毒合併感染組與人類免疫缺陷病毒/乙型肝炎病毒/丙型肝炎病毒三重感染組的血漿IL-27濃度差異顯著。我們還發現人類免疫缺陷病毒單獨感染組中，血漿IL-27濃度與CD4⁺ T 淋巴細胞數量顯著正相關 (r = 0.177, P = 0.034)。 / 我們進一步分析了人類免疫缺陷病毒和丙型肝炎病毒的病毒載量對血漿IL-27濃度的影響，發現HIV單獨感染組中人類免疫缺陷病毒載量與血漿IL-27濃度沒有顯著相關 (r = - 0.063, P = 0.679)，而人類免疫缺陷病毒/丙型肝炎病毒合併感染組中，人類免疫缺陷病毒載量與血漿IL-27濃度顯著正相關 (r = 0.362, P = 0.049)。人類免疫缺陷病毒/丙型肝炎病毒合併感染組中，人類免疫缺陷病毒載量與丙型肝炎病毒載量缺少顯著線性關聯 (r = - 0.072, P = 0.704)，而人類免疫缺陷病毒/丙型肝炎病毒合併感染組可根據人類免疫缺陷病毒與丙型肝炎病毒的病毒載量再細分成血漿IL-27濃度差異顯著的三組 (P = 0.014) ， 丙型肝炎病毒載量與血漿IL-27濃度缺少顯著關聯 (r = - 0.119, P = 0.530) 。 / 我們利用TaqMan®等位基因分型技術測定深圳男同性戀人群中IL-27 p28基因的單核苷酸多態性 (SNP)。結果顯示，人類免疫缺陷病毒感染組IL-27 p28 -964A/G 和4603G/A的基因型與健康男同性戀參照組的基因型沒有顯著差異， IL-27 p28 -964A/G 和4603G/A的等位基因比率也沒有顯著差異。結果也顯示，IL-27 p28 2905T/G的TG基因型可減少2.77倍的人類免疫缺陷病毒感染風險，等位基因G可減少2.72倍的人類免疫缺陷病毒感染風險。連鎖不平衡在IL-27 p28 -964A/G 和2905T/G 中存在 ( / 綜上所述， 在本研究中，我們首次調查了深圳人類免疫缺陷病毒，乙型肝炎病毒，丙型肝炎病毒合併感染的流行情況，並分析了合併感染的風險因素。 發現人類免疫缺陷病毒單獨感染者，人類免疫缺陷病毒/乙型肝炎病毒合併感染者， 及人類免疫缺陷病毒/丙型肝炎病毒合併感染者的血漿IL-27濃度比健康參照組顯著地升高；人類免疫缺陷病毒單獨感染組中，血漿IL-27濃度與CD4⁺ T淋巴細胞數量顯著正相關。人類免疫缺陷病毒/丙型肝炎病毒合併感染組中，人類免疫缺陷病毒載量與血漿IL-27濃度顯著正相關 (r = 0.362, P = 0.049)。分析深圳男同性戀人群IL-27 p28基因的單核苷酸多態性，發現IL-27 p28 2905T/G 與人類免疫缺陷病毒感染相關，GGG單型可降低男同性戀人群人類免疫缺陷病毒感染的風險。 / Human Immunodeficiency Virus (HIV) is the causative agent of Acquired Immunodeficiency Syndrome (AIDS); HIV/AIDS caused 1.8 million deaths world-widely in 2010 and became a major global health challenge. HIV co-infections with Hepatitis B virus (HBV), Hepatitis C virus (HCV) are common and have emerged into new health problems with severe clinical consequences. Since the discovery of HIV, massive progress in understanding of the pathogen has been achieved. Due to the restriction of research model, how human immune system responds to HIV infection, particularly, to HBV or HCV co-infections is still worthy further elucidation. / A cohort study was first conducted in Shenzhen regarding the seroprevalence of HBV, HCV infections among HIV-infected population. Totally 914 HIV positive individuals were recruited in the study and tested for HBsAg and anti-HCV antibodies. The results showed a 10.9% (100/914) HIV/HBV co-infection rate, 14.6% (133/914) HIV/HCV co-infection prevalence and 3.7% (34/914) HIV/HBV/HCV triple-infection prevalence. Multivariate logistic regression revealed that HIV transmission risk behavior was significantly associated with HIV, HBV, HCV co-infections. Most HIV/HBV co-infection cases got HIV through sexual contact including heterosexual and homosexual behaviors (95/100, 95%); while most HIV/HCV co-infection subjects were injection drug users (IDUs) (89/133, 66.9%). In the case of HIV/HBV/HCV triple-infection, IDUs accounted for a large ratio (28/34, 82.4%). Among IDUs, most of them were male (108/122, 88.5%) and nearly half were aged 27 to 32 years old (56/122, 45.9%). Near half people who got HIV through blood and blood products were HIV/HCV co-infected (10/23, 43.5%). Gender has a significant correlation with HIV risk behavior and most IDUs were male. / Next, we applied ELISA to test HIV positive clinical samples and proved that plasma interleukin-27 (IL-27) level was significantly elevated in HIV mono-infected, HIV/HBV co-infected and HIV/HCV co-infected subjects when compared with healthy controls. Later, we further revealed that plasma IL-27 titer was not significantly varied among HIV, HBV and HCV co-infections except between HIV/HCV co-infections and HIV/HBV/HCV triple-infections. We also observed a significant positive correlation between CD4⁺ T cell counts and plasma IL-27 titer within HIV mono-infected group (r = 0.177, P = 0.034). / We further analyzed the impact HIV and HCV viral loads on plasma IL-27 titer. We found there was no significant correlation between HIV viral load and IL-27 titer among HIV mono-infected individuals (r = - 0.063, P = 0.679); while a significant positive correlation was observed between HIV viral load and IL-27 titer in HIV/HCV co-infected individuals (r = 0.362, P = 0.049). In the case of HIV/HCV co-infection, there was no significant linear correlation between HIV and HCV viral loads (r = - 0.072, P = 0.704) but exist obvious subdivision of samples in terms of HIV and HCV viral loads with significant IL-27 titer variance (P = 0.014). No correlation was observed between HCV viral load and IL-27 titer (r = - 0.119, P = 0.530). / IL-27 p28 polymorphisms were genotyped with TaqMan® Allelic Discrimination Assay in Chinese men who have sex with men (MSM) population in Shenzhen and the results revealed that proportions of IL-27 p28 -964A/G and 4603G/A genotypes were not significantly different from the healthy controls; IL-27 p28 -964A/G and 4603G/A allele frequencies were similar between HIV positive MSM group and healthy control MSM group. Results also showed that for IL-27 p28 2905T/G polymorphism, TG genotype has a 2.77-fold decreased risk of HIV susceptibility and subjects with G allele has a 2.72-fold decreased risk of HIV susceptibility. Linkage disequilibrium (LD) coefficients were observed between IL-27 p28 -964A/G and 2905T/G ( / In conclusion, the seroprevalences of HBV and HCV infection among HIV positive population in Shenzhen were surveyed and risk factors associated with co-infections were analyzed. Plasma IL-27 titer was significantly elevated in HIV mono-infected, HIV/HBV co-infected and HIV/HCV co-infected individuals. IL-27 level was correlated with CD4⁺ T cell counts within HIV mono-infected people. A significant positive correlation was found between HIV viral load and IL-27 titer in HIV/HCV co-infected individuals (r = 0.362, P = 0.049). IL-27 p28 2905T/G was associated with individual susceptibility to HIV infection and haplotype GGG showed a protective role in restricting HIV infection in MSM population. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / He, Lai. / "October 2012." / Thesis (Ph.D.)--Chinese University of Hong Kong, 2013. / Includes bibliographical references (leaves 135-155). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstract also in Chinese. / Abstract (English) --- p.iii / Abstract (Chinese) --- p.vi / Acknowledgements --- p.ix / Contents --- p.x / List of Tables --- p.xv / List of Figures --- p.xvi / Abbreviations --- p.xvii / Chapter Chapter 1 --- Introduction --- p.1 / Chapter 1.1 --- Human Immunodeficiency Virus --- p.1 / Chapter 1.1.1 --- HIV virology --- p.1 / Chapter 1.1.1.1 --- HIV structure and genome organization --- p.1 / Chapter 1.1.1.2 --- HIV life cycle --- p.3 / Chapter 1.1.1.3 --- HIV genotypes --- p.5 / Chapter 1.1.2 --- HIV epidemiology --- p.6 / Chapter 1.1.2.1 --- Global HIV epidemiology --- p.6 / Chapter 1.1.2.2 --- HIV epidemiology in China --- p.9 / Chapter 1.1.3 --- HIV pathogenesis --- p.13 / Chapter 1.1.3.1 --- Natural history of HIV infection --- p.13 / Chapter 1.1.3.2 --- HIV transmission --- p.15 / Chapter 1.1.3.3 --- HIV tropism --- p.17 / Chapter 1.1.4 --- Immune responses to HIV infection --- p.19 / Chapter 1.1.4.1 --- Innate immune response --- p.19 / Chapter 1.1.4.2 --- Adaptive immune response --- p.21 / Chapter 1.1.5 --- Diagnosis --- p.24 / Chapter 1.1.6 --- HIV prevention --- p.25 / Chapter 1.1.7 --- Anti-HIV therapy --- p.25 / Chapter 1.1.8 --- Hepatitis B virus, Hepatitis C virus infection --- p.26 / Chapter 1.1.8.1 --- HBV infection natural history, diagnosis, disease progression and epidemiology --- p.26 / Chapter 1.1.8.2 --- HCV infection natural history, diagnosis, disease progression and epidemiology --- p.30 / Chapter 1.1.9 --- HIV, HBV, HCV co-infections --- p.32 / Chapter 1.2 --- Interleukin-27 --- p.36 / Chapter 1.2.1 --- Biology of IL-27 --- p.36 / Chapter 1.2.2 --- IL-27 on immune system --- p.37 / Chapter 1.2.3 --- IL-27 anti-tumor properties --- p.38 / Chapter 1.2.4 --- IL-27 antiviral features --- p.40 / Chapter 1.2.5 --- IL-27 with hepatitis --- p.41 / Chapter 1.3 --- Single-nucleotide polymorphisms (SNPs) --- p.42 / Chapter 1.3.1 --- Types of SNPs --- p.43 / Chapter 1.3.2 --- Functions of SNPs --- p.43 / Chapter 1.4 --- Objectives of the study --- p.45 / Chapter Chapter 2 --- Seroprevalence of HBV, HCV infection among HIV positive individuals in Shenzhen --- p.52 / Chapter 2.1 --- Introduction --- p.52 / Chapter 2.2 --- Materials and methods --- p.54 / Chapter 2.2.1 --- Study participants --- p.54 / Chapter 2.2.2 --- Measure of HBV, HCV seroprevalence --- p.55 / Chapter 2.2.3 --- Statistical analysis --- p.60 / Chapter 2.3 --- Results --- p.61 / Chapter 2.3.1 --- HIV infection in Shenzhen --- p.61 / Chapter 2.3.2 --- Seroprevalence of HBV, HCV infection among HIV positive individuals in Shenzhen --- p.61 / Chapter 2.4 --- Discussion --- p.65 / Chapter 2.4.1 --- HIV infection in Shenzhen --- p.65 / Chapter 2.4.2 --- HIV, HBV, HCV co-infections in Shenzhen --- p.68 / Chapter 2.4.3 --- Limitations of the study --- p.71 / Chapter Chapter 3 --- Upregulation of Interleukin-27 titer in HIV infected persons --- p.78 / Chapter 3.1 --- Introduction --- p.78 / Chapter 3.2 --- Materials and methods --- p.80 / Chapter 3.2.1 --- Study participants --- p.80 / Chapter 3.2.2 --- Measure of HIV, HBV, HCV infection --- p.80 / Chapter 3.2.3 --- Detection of IL-27 in plasma --- p.81 / Chapter 3.2.4 --- CD4 counting --- p.84 / Chapter 3.2.5 --- Statistical analysis --- p.84 / Chapter 3.3 --- Results --- p.84 / Chapter 3.3.1 --- Demographics of study participants --- p.84 / Chapter 3.3.2 --- Upregulation of IL-27 levels in HIV infected persons --- p.85 / Chapter 3.3.3 --- Correlation of plasma IL-27 titer with CD4⁺ T cell count --- p.86 / Chapter 3.4 --- Discussion --- p.86 / Chapter Chapter 4 --- Impact of HIV, HCV viral loads on Interleukin-27 titer among Antiretroviral Therapy- Naïve HIV positive Chinese --- p.95 / Chapter 4.1 --- Introduction --- p.95 / Chapter 4.2 --- Materials and methods --- p.96 / Chapter 4.2.1 --- Study participants --- p.97 / Chapter 4.2.2 --- HIV, HBV and HCV Serological assays --- p.97 / Chapter 4.2.3 --- CD4 counting --- p.97 / Chapter 4.2.4 --- Detection of plasma IL-27 --- p.98 / Chapter 4.2.5 --- Quantification of HIV, HCV viral loads --- p.98 / Chapter 4.2.6 --- Statistical analysis --- p.102 / Chapter 4.3 --- Results --- p.102 / Chapter 4.3.1 --- Demographics of study participants --- p.102 / Chapter 4.3.2 --- Plasma IL-27 was elevated in HIV-positive persons --- p.103 / Chapter 4.3.3 --- Correlation of IL-27 titer and CD4⁺ T cell count --- p.103 / Chapter 4.3.4 --- Correlation of HIV viral load and IL-27 titer --- p.104 / Chapter 4.3.5 --- Correlation of HCV viral load and IL-27 titer --- p.104 / Chapter 4.4 --- Discussion --- p.105 / Chapter Chapter 5 --- Association of Interleukin-27 polymorphisms with the susceptibility to HIV infection in a Chinese men who have sex with men population --- p.116 / Chapter 5.1 --- Introduction --- p.116 / Chapter 5.2 --- Materials and methods --- p.118 / Chapter 5.2.1 --- Study participants --- p.118 / Chapter 5.2.2 --- HIV screening --- p.118 / Chapter 5.2.3 --- Genomic DNA extraction --- p.119 / Chapter 5.2.4 --- IL-27 p28 -964A/G, 2905T/G and 4603G/A genotyping --- p.120 / Chapter 5.2.5 --- Statistical analysis --- p.121 / Chapter 5.3 --- Results --- p.122 / Chapter 5.3.1 --- Demographics of study participants --- p.122 / Chapter 5.3.2 --- IL-27 genotypes and allele frequencies in HIV MSM and healthy MSM controls --- p.122 / Chapter 5.3.3 --- LD analysis and haplotype analysis --- p.123 / Chapter 5.4 --- Discussion --- p.124 / Chapter Chapter 6 --- Summary and perspectives --- p.130 / Chapter 6.1 --- Summary --- p.130 / Chapter 6.2 --- Perspectives --- p.132 / Bibliography --- p.135

published_or_final_version / Medicine / Master / Doctor of Medicine

Zhu, Lin. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2007. / Includes bibliographical references (leaves 103-118). / Abstracts in English and Chinese. / Contents --- p.I / List of Abbreviations --- p.IV / List of Tables and Figures --- p.V / Chapter Chapter One: --- Introduction --- p.1 / Chapter 1.1 --- Viral Hepatitis --- p.2 / Chapter 1.2 --- Global Epidemiology of HBV --- p.3 / Chapter 1.3 --- Modes of Transmission --- p.4 / Chapter 1.4 --- Diagnostic Tests --- p.5 / Chapter 1.4.1 --- HBeAg and Anti-HBe --- p.7 / Chapter 1.4.2 --- Serum Enzymes --- p.8 / Chapter 1.4.3 --- HBV DNA Assays --- p.9 / Chapter 1.4.3.1 --- HBV DNA Assays --- p.9 / Chapter 1.4.3.2 --- Clinical Applications of DNA Assays --- p.10 / Chapter 1.4.4 --- Histology --- p.13 / Chapter 1.5 --- Natural Course of Chronic Hepatitis infection --- p.18 / Chapter 1.5.1 --- Phases of chronic hepatitis B --- p.18 / Chapter 1.5.2 --- HBeAg-negative chronic hepatitis B --- p.21 / Chapter 1.6 --- Molecular biology of HBV --- p.23 / Chapter 1.6.1 --- Overview --- p.23 / Chapter 1.6.2 --- Genomic structure and organization --- p.24 / Chapter 1.6.2.1 --- Surface ORF --- p.24 / Chapter 1.6.2.2 --- Precore/Core ORF --- p.25 / Chapter 1.6.2.3 --- Polymerase ORF --- p.25 / Chapter 1.6.2.4 --- X ORF --- p.26 / Chapter 1.7 --- Genetic Variation of HBV --- p.31 / Chapter 1.7.1 --- HBV genotypes --- p.31 / Chapter 1.7.2 --- Predominant genotypes and their subgroups in Asia --- p.33 / Chapter 1.7.3 --- HBV mutations --- p.36 / Chapter 1.7.3.1 --- Precore mutations --- p.37 / Chapter 1.7.3.2 --- Core promoter mutations --- p.38 / Chapter 1.7.3.3 --- Other Mutations associated with clinical outcome --- p.40 / Chapter Chapter Two: --- Methodology --- p.44 / Chapter 2.1 --- Aims and Hypothesis --- p.45 / Chapter 2.1.1 --- Aims --- p.46 / Chapter 2.1.2 --- Hypothesis --- p.47 / Chapter 2.2 --- Patient Recruitment --- p.48 / Chapter 2.3 --- Laboratory Assays --- p.49 / Chapter 2.3.1 --- Preparation of serum HBV DNA --- p.49 / Chapter 2.3.2 --- Quantification of serum HBV DNA --- p.51 / Chapter 2.4 --- Full-genome Amplification of HBV DNA --- p.53 / Chapter 2.5 --- Full-genome Sequencing of HBV DNA --- p.55 / Chapter 2.6 --- Assembly of HBV Full-genome Sequence --- p.58 / Chapter 2.7 --- Phylogenetic Analysis --- p.59 / Chapter 2.7.1 --- Construction of phylogenetic tree --- p.59 / Chapter 2.7.2 --- Genotype and subgenotype determination --- p.60 / Chapter 2.8 --- HBV Mutations --- p.62 / Chapter 2.9 --- Info-gain program --- p.64 / Chapter 2.10 --- Statistical Analysis --- p.65 / Chapter Chapter Three: --- Results --- p.67 / Chapter 3.1 --- Patient Information --- p.68 / Chapter 3.2 --- Phylogenetic Analysis --- p.69 / Chapter 3.3 --- HBV genotypes/subgenotypes --- p.76 / Chapter 3.4 --- “Hot-spo´tح HBV Mutants --- p.79 / Chapter 3.5 --- HBV Mutation Associated with Liver Fibrosis --- p.82 / Chapter 3.5.1 --- Mutant selection --- p.82 / Chapter 3.5.2 --- Clinical significance of novel mutants --- p.84 / Chapter Chapter Four: --- Discussion --- p.88 / Chapter 4.1 --- Full-genome Sequencing Strategy --- p.89 / Chapter 4.2 --- HBV genotypes/subgenotypes Distribution and Disease Activity --- p.90 / Chapter 4.2.1 --- HBV genotypes/subgenotypes distribution --- p.90 / Chapter 4.2.2 --- Clinical significance of genotypes/subgenotypes --- p.91 / Chapter 4.3 --- HBV Hotspot Mutants and Disease Activity --- p.93 / Chapter 4.4 --- HBV Novel Mutants --- p.96 / Chapter 4.5 --- Limitation of the Study and Future Work --- p.97 / Chapter 4.5.1 --- Limitation --- p.97 / Chapter 4.5.2 --- Future Direction --- p.98 / Chapter Chapter Five: --- Conclusions --- p.99 / References --- p.102

近年来，针对就业和就学中遭遇歧视的困境，中国乙肝携带者发起一场要求消除歧视、维护合法权益的抗争运动。为什么乙肝携带者就业歧视问题在中国如此显著？面对国家和市场这两大最具权势的系统，公民社会将何以对抗？本文旨在从社会学的视角对这场“将‘乙肝’去除"的运动进行解读。 / 本文采用个案研究方法，以北京益仁平中心为主要研究对象，围绕 “乙肝"在中国的建构和重构过程，将研究聚焦于三个方面：第一，乙肝污名化过程以及国家、市场中的话语权；第二，反乙肝歧视维权运动的条件和动员机制；第三，“将‘乙肝’去除"中的政治和权力话语三角。 / 本文从社会运动理论中的资源动员、政治机会结构和框架理论出发解读中国乙肝携带者的维权运动；将运动中的微观景象与宏观社会结构结合起来，考察影响乙肝携带者维权运动的主要因素以及运动的动员机制。研究伊始分别从国家和市场两个领域审视乙肝歧视问题在中国的建构过程，阐明乙肝污名化是政府权威以及市场中医药商和医学权威共谋下的合力作用，从而为乙肝携带者反歧视抗争运动的后续研究选择一个合适的立足点。笔者在案例中发现，组织在维权运动中将乙肝携带者群体动员起来，采取有效的策略，充分利用其在资源获得方面的优势、建立乙肝维权组织网络、善于把握时机营造政治机会空间、并能够吸纳律师和媒体的专业力量是维权行动能取得成功的重要因素。 / 组织在维权行动中的话语框架对运动的发展至关重要。乙肝携带者群体对组织运动框架的认同是动员成功的基础；掌握定义“乙肝"的主动权、运动领袖的可信性、框架话语表达的日常化、与媒体的良好关系等策略有助于框架在动员中与参与者、旁观者产生共鸣；抗争精英通过话语框架为抗争活动提供合法性。 / 反乙肝歧视维权运动可以看作是一个“将‘乙肝’去除"的“去污名化"运动。一方面，中央政府与地方政府有着各自自主性利益；另一方面，乙肝携带者群体内部就抗争形式也难以统一，这两种分裂情况交叉形成了一个围绕“将‘乙肝’去除"的，以规则、效益和权利为话语的权力三角，支撑反歧视行动的抗争空间。权力三角的多变性决定去除“乙肝"的行动是有策略的、冒险的，但却相对稳定。 / Hepatitis B Virus carriers (HBVers) have launched series social movements targeting at eliminating discriminations against HBVers in job market and promoting fair employment in recent decade of years. Why does nowhere match the HBV discrimination in such country like China? How is contentious politics possible when the powerless engage in struggles with power holders, like state and market in China? The thesis attempts to learn the intricacies of body politics with sociological approaches. / Yirenping, a NGO located in Beijing, is selected as research object in this case study. Concentrating on the political nature of the HBV confrontations, this thesis is comprised of three parts: first, the stigmatization of HBV in China; second, tactics and strategies that employed against the system of discrimination; third, the politics of “Removing HBV" and the power triangle among state, market and civil society. / The analysis of the HBV movement is informed by three sociological theories of social movements: resource mobilization, political opportunity structure and framing, meanwhile macro structure and micro interaction are combined. It is postulated that this disease discrimination in China occurs when confronting an entrenched stigmatization conjoined from both state and market dedicated to keeping the HBVers excluded and marginalized, which serves as a departure point for further analysis of the struggles for power against this discrimination. Resources mobilized, leaderships and organizations, networks among HBVers and outside supporters, strategies in mobilization positively facilitate the anti-discrimination movements. Utilizing the institutional advocacies as well as informal networks with officials, NPC & CPCCC delegates open more political opportunities within the preexisting political environment. / Framing is essential to the movement mobilization. Identifying closely with the visions and missions in movements, the self conceptualization of HBV-discrimination, charismatic leaders, the everyday narrative of the frame, as well as strategic media coverage help promoting resonance among movement participants and standers-by. Framing strategies provide legitimacy for HBV selves in collective movements. / Finally, the thesis came to the conclusion that anti-discrimination-against-HBVers social movements in China can be interpreted as a process of struggle to “Removing HBV" power. Central government and local ones have their autonomies and interests respectively, while weak but observed divisions in protesting strategies also exist within the HBVers, which shape a triangle of power struggles among the dominant and dominated groups. The power triangle is flexible, and the “Removing HBV" movements are strategic, risk-taking, while being routinized. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / 郭娜. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2013. / Includes bibliographical references (leaves 137-156) / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstracts in Chinese and English. / Guo Nuo. / 中文摘要 --- p.i / 英文摘要 --- p.ii / 引言 --- p.1 / Chapter 第一章 --- 导论 乙肝：作为医学问题和作为社会问题 --- p.3 / Chapter 1.1 --- 作为医学问题的乙型肝炎及其全球地理分布 --- p.3 / Chapter 1.2 --- 乙型肝炎在中国 --- p.6 / Chapter 1.3 --- 作为社会问题的乙肝歧视 --- p.8 / Chapter 1.4 --- 研究方法 --- p.10 / Chapter 1.5 --- 小结 --- p.14 / Chapter 第二章 --- 研究问题与文献回顾 --- p.15 / Chapter 2.1 --- 社会运动理论的发展脉络 --- p.16 / Chapter 2.2 --- 认同与社会运动的动员 --- p.21 / Chapter 2.3 --- 中国底层社会与维权抗争研究回顾 --- p.24 / Chapter 2.4 --- 中国反乙肝歧视运动的分析框架 --- p.26 / Chapter 2.5 --- 小结 --- p.34 / Chapter 第三章 --- 政府与入职体检 --- p.35 / Chapter 3.1 --- 新中国成立之初的公共卫生政策 --- p.35 / Chapter 3.2 --- 中国人事制度改革和公务员职业声望 --- p.39 / Chapter 3.3 --- 体检标准与强制乙肝检测 --- p.43 / Chapter 3.4 --- 小结 --- p.47 / Chapter 第四章 --- 市场话语权与定义“乙肝" --- p.49 / Chapter 4.1 --- 市场中的虚假广告 --- p.50 / Chapter 4.2 --- 体检经济 --- p.54 / Chapter 4.3 --- 医药商与医学权威 --- p.56 / Chapter 4.4 --- 小结 --- p.58 / Chapter 第五章 --- 乙肝携带者的个人经验 --- p.61 / Chapter 5.1 --- 疾病的社会建构 --- p.62 / Chapter 5.2 --- 乙肝携带者的认知过程 --- p.66 / Chapter 5.3 --- 乙肝携带者的抗争选择 --- p.68 / Chapter 5.4 --- 小结 --- p.74 / Chapter 第六章 --- 从个体经验到集体行动：公民社会的回应 --- p.76 / Chapter 6.1 --- 从个人困境到集体行动 --- p.76 / Chapter 6.2 --- 反乙肝歧视运动中的资源动员 --- p.80 / Chapter 6.3 --- 反乙肝歧视组织网络 --- p.82 / Chapter 6.4 --- 反乙肝歧视运动中的机会空间 --- p.86 / Chapter 6.5 --- 小结 --- p.90 / Chapter 第七章 --- 框架策略：反乙肝歧视运动中的动员 --- p.91 / Chapter 7.1 --- 认同与社会运动 --- p.91 / Chapter 7.2 --- 反乙肝歧视运动的行动框架 --- p.95 / Chapter 7.3 --- 反乙肝歧视运动的动员策略 --- p.100 / Chapter 7.4 --- 小结 --- p.107 / Chapter 第八章 --- 身体的政治：将“乙肝"去除 --- p.108 / Chapter 8.1 --- 权力的维度 --- p.108 / Chapter 8.2 --- 反乙肝歧视行动的抗争轨迹 --- p.111 / Chapter 8.3 --- 国家、市场与公民社会：将“乙肝"去除 --- p.116 / Chapter 8.4 --- 小结 --- p.130 / Chapter 第九章 --- 总结与讨论 --- p.131 / 参考文献 --- p.137 / Chapter 附录A --- 访谈提纲 --- p.157 / Chapter 附录B --- 64名被访者基本信息概况 --- p.160 / 致谢 --- p.162