SARS病人的免疫应答

机体抵御SARS-CoV的免疫应答包括非特异性和特异性两类。非特异性免疫应答主要包括细胞因子和NK细胞对病毒的抑制和杀伤作用等。特异性免疫反应包括体液免疫和细胞免疫。体液免疫反应是指当SARS-CoV感染机体后，引起B淋巴细胞的活化，其中一些细胞迅速分化为浆细胞，分泌IgM；而另一些细胞在T细胞和细胞因子的辅助下，发生类型转换，     

与宫颈癌相关的人乳头瘤病毒的持续感染与免疫逃逸

人乳头瘤病毒是宫颈癌的病原体.机体的免疫应答不能清除上皮细胞内整合感染的乳头瘤病毒,该病毒持续感染是宫颈癌发生的原因.免疫逃逸是病毒自身因素和机体免疫因素综合的结果.病毒隐匿、病毒癌蛋白、细胞因子、粘附分子等参与病毒的免疫逃逸.     

与宫颈癌相关的人乳头瘤病毒的持续感染与免疫逃逸

人乳头瘤病毒是宫颈癌的病原体。机体的免疫应答不能清除上皮细胞内整合感染的乳头瘤病毒，该病毒持续感染是宫颈癌发生的原因。免疫逃逸是病毒自身因素和机体免疫因素综合的结果。病毒隐匿、病毒癌蛋白、细胞因子、粘附分子等参与病毒的免疫逃逸。     

乙型肝炎特异性细胞免疫的研究

本文运用白细胞粘附抑制试验(LAI)研究了乙型肝炎患者外周血特异性细胞免疫反应。共检262例,分8个实验组。乙型肝炎患者HBsAg都阳性。研究结果表明:1.急性乙型肝炎可分为两种类型,即抗原清除型和抗原持续型。本文分别绘制了它们的细胞免疫动态曲线。前者,病毒的清除大多发生在疾病发作后二个月之内,在此阶段,细胞免疫阴性,病毒清除后,细胞免疫水平迅速上升,并持续两个月而消失。后者,其曲线相似于抗原清除型,但变化幅度较小。2.乙型肝炎的慢性持续状态可能是由机体和病毒两方面的因素所造成,即机体的免疫耐受和病毒基因在肝细胞膜上表达的变化。3.在乙型肝炎的免疫保护中,乙型肝炎病毒的清除是细胞免疫和体液免疫协同作用的结果。     

机体对人乳头状瘤病毒感染的免疫反应研究进展

机体可对人乳头状瘤病毒蛋白或病毒样粒子产生抗体,表皮细胞可产生多种细胞因子参与对病毒的非特异性细胞免疫反应,而机体对人乳头状瘤病毒的特异性细胞免疫反应要经过识别和效应阶段,人乳头状瘤病毒通过几个可能的机制逃逸机体的免疫反应。     

严重急性呼吸综合症特异性记忆T细胞的研究进展

严重急性呼吸综合症（SARS）冠状病毒可以同时诱导出体液免疫应答和细胞免疫应答。对SARS康复者血清中特异性抗体水平检测表明,其随时间推移明显降低。特异性细胞免疫应答在机体清除病毒的过程中发挥着重要的作用,尤其是特异性记忆T细胞在抵御病毒再次入侵时,能迅速产生免疫应答有效保护机体。     

严重急性呼吸综合症特异性记忆T细胞的研究进展

严重急性呼吸综合症(SARS)冠状病毒可以同时诱导出体液免疫应答和细胞免疫应答.对SARS康复者血清中特异性抗体水平检测表明,其随时间推移明显降低.特异性细胞免疫应答在机体清除病毒的过程中发挥着重要的作用,尤其是特异性记忆T细胞在抵御病毒再次入侵时,能迅速产生免疫应答有效保护机体.     

天然免疫分子APOBEC3G蛋白的抗HBV研究进展

天然免疫分子APOBEC3G蛋白酶是一种胞苷脱氨酶,是机体固有免疫反应的新成员,参与宿主抵抗病毒入侵的天然免疫防御机制,具有较强的广谱抗逆转录病毒能力。APOBEC3G抗逆转录病毒的作用机制研究已成为机体固有免疫研究新靶点,为机体固有免疫机制的研究开拓了新的方向。由于APOBEC3G可能在基因超突变、病毒脱衣壳、HBV RNA的逆转录、HBV DNA复制、HBV DNA核壳化等多方面影响HBV复制,所以研究APOBEC3G的抗病毒作用是治疗HBV感染的研究重点,也有可能对其他病毒性疾病的防治提供新的线索并产生重要的影响。     

CD4+CD25+调节性T细胞和TLRs在幽门螺杆菌 免疫逃逸中的作用

宿主感染幽门螺杆菌(H.pylori)后,会产生炎症反应和免疫反应,但宿主不能完全清除H.pylori,原因之一为H.pylori可逃逸宿主免疫形成持续慢性感染。H.pylori免疫逃逸机制尚不明确,目前此机制研究热点为CD4+CD25+调节性T细胞和TLRs在H.pylori免疫逃逸中的作用。     

特异性细胞毒T淋巴细胞清除胞内乙肝病毒机制的研究进展

乙型肝炎病毒 (HBV)是一种有胞膜、无胞毒活性的、双链DNA嗜肝病毒。正常情况下, 大多数免疫功能健全的成人感染HBV后可通过天然免疫和适应性免疫应答的协调作用清除之, 并可获得对HBV再次感染的抵抗力。但约有 5%的HBV感染者或经垂直途径感染HBV的人群不能有效清除感染的HBV, 导致病毒的持续感染, 有的人甚至最终发展为肝硬化或肝癌。已有的研究表明: 机体针对病毒所产生的特异性细胞免疫应答可能是清除机体内病毒的重要因素 [1]。因而本文拟就病毒特异性细胞毒T淋巴细胞清除乙肝病毒机制的近期研究进展作一综述。1　特异性T…     

Hepatitis C virus--T-cell responses and viral escape mutations

Hepatitis C virus (HCV) is a small, enveloped RNA virus and the number of HCV-infected individuals worldwide is estimated to be approximately 170 million. Most HCV infections persist, with up to 80% of all cases leading to chronic hepatitis associated with liver fibrosis, cirrhosis, and hepatocellular carcinoma. HCV-host interactions have a crucial role in viral survival, persistence, pathogenicity of infection, and disease progression. Maintenance of a vigorous, sustained cellular immune response recognizing multiple epitopes is essential for viral clearance. To escape immune surveillance, HCV alters its epitopes so that they are no-longer recognized by T cells and neutralizing antibodies, in addition to interfering with host cell cellular components and signaling pathways. The generation of escape variants is one of the most potent immune evasion strategies utilized by HCV. A large body of evidence suggests that single or multiple mutations within HLA-restricted epitopes contribute to viral immune escape and establishment of viral persistence. Further elucidation of the molecular mechanisms underlying immune escape will aid in the design of novel vaccines and therapeutics for the disease.     

Interaction of human papillomaviruses with the host immune system: a well evolved relationship

Human papillomavirus (HPV) infections are generally long lasting, and a host immune response to infection is hard to detect. Nevertheless immunocompromised subjects control HPV infection less well than those with intact immunity. Immune responses are best documented for the papillomavirus groups that cause evident human disease, particularly those responsible for anogenital cancers and genital warts. Humoral immunity to the viral capsid has been shown sufficient for protection against infection, while innate and adaptive cell mediated immunity appears important for eventual elimination of HPV infection. However, molecular and cellular mechanisms responsible for protection from and clearance of HPV infection are not completely established.     

Respiratory syncytial virus infection: immune response, immunopathogenesis, and treatment

Respiratory syncytial virus (RSV) is the single most important cause of lower respiratory tract infection during infancy and early childhood. Once RSV infection is established, the host immune response includes the production of virus-neutralizing antibodies and T-cell-specific immunity. The humoral immune response normally results in the development of anti-RSV neutralizing-antibody titers, but these are often suboptimal during an infant's initial infection. Even when the production of RSV neutralizing antibody following RSV infection is robust, humoral immunity wanes over time. Reinfection during subsequent seasons is common. The cellular immune response to RSV infection is also important for the clearance of virus. This immune response, vital for host defense against RSV, is also implicated in the immunopathogenesis of severe lower respiratory tract RSV bronchiolitis. Many details of the immunology and immunopathologic mechanisms of RSV disease known at present have been learned from rodent models of RSV disease and are discussed in some detail. In addition, the roles of immunoglobulin E, histamine, and eosinophils in the immunopathogenesis of RSV disease are considered. Although the treatment of RSV bronchiolitis is primarily supportive, the role of ribavirin is briefly discussed. Novel approaches to the development of new antiviral drugs with promising anti-RSV activity in vitro are also described.     

Manipulation of immune responses by Epstein-Barr virus

Epstein-Barr virus (EBV) infects and persists for life in the majority of the human population. Persistence is achieved through a combination of strictly regulated programs of latent infection in B-cells and chronic reactivation of virus replication in lymphoid tissue and mucosal surfaces. The resulting multiple patterns of virus-host interaction have selected unique strategies of immune escape. T-cell mediated immunity plays a central role in the control of EBV latency and several immune escape mechanism that protect the virus at this stage of its life circle have been characterized in details. In contrast, the contribution of innate immunity and the immune regulation of productive infection are largely unexplored areas that may yield important clues on the establishment and maintenance of EBV persistence. This review summarizes well known and emerging mechanisms of EBV immune escape that may reveal new strategies of immunoregulation and promote new approaches to the prophylaxis and treatment of EBV associated diseases.     

Local immunosuppression induced by high viral load of human papillomavirus: characterization of cellular phenotypes producing interleukin‐10 in cervical neoplastic lesions

A specific immune response to human papillomavirus (HPV) in the cervical microenvironment plays a key role in eradicating infection and eliminating mutated cells. However, high‐risk HPVs modulate immune cells to create an immunosuppressive microenvironment, and induce these immune cells to produce interleukin 10 (IL‐10). This production of IL‐10, in conjunction with HPV infection, contributes to the appearance of cervical neoplastic lesions. We sought to characterize the IL‐10‐producing cellular phenotype, and investigate the influence of host and HPV factors upon the induction of an immunosuppressive microenvironment. Immunohistochemical analysis demonstrated an increase in IL‐10 production by keratinocytes, macrophages and Langerhans cells in high‐grade cervical lesions and cervical cancer. This increase was more pronounced in patients older than 30 years, and was also correlated with high viral load, and infection with a single HPV type, particularly high‐risk HPVs. Our results indicate the existence of a highly immunosuppressive microenvironment composed of different IL‐10‐producing cellular phenotypes in cervical cancer samples, and samples classified as high‐grade cervical lesions (cervical intraepithelial neoplasia stages II and III). The immunosuppressive microenvironment that developed for these different cellular phenotypes favours viral persistence and neoplastic progression.     

Modulation of dendritic cell function by persistent viruses

Worldwide, chronic viral infections cause major health problems with severe morbidity and mortality. HIV and hepatitis C virus (HCV) manifest themselves as persistent infections, but they are entirely distinct viruses with distinct replication mechanisms, tropism, and kinetics. Coinfections with HCV among people with HIV are emerging as a growing problem. Cellular immune responses play an important role in viral clearance and disease pathogenesis. However, cellular immunity to HIV and HCV is affected severely in chronic patients. Various hypotheses have been proposed to explain the dysfunctional T cell response, including viral escape mutations, exhaustion of the T cell compartment, and the activity of regulatory T cells. Also, modulation of the function of dendritic cells (DC) has been suggested as one of the mechanisms used by persistent viruses to evade the immune system. In this review, we will focus on DC interactions with one murine persistent virus (lymphocytic choriomeningitis virus clone 13) and two human persistent viruses (HIV-1 and HCV), intending to examine if general strategies are used by persistent viruses to modulate the function of DC to improve our understanding of the mechanisms underlying the development and maintenance of viral persistence.     

HLA与HPV相关肿瘤的研究进展

人乳头状瘤病毒（HPV）感染是宫颈癌等肿瘤的高危因素,其致瘤机制尚未完全阐明。在免疫应答过程中,机体HLA-I,Ⅱ,Ⅲ类分子表达异常与HPV相关肿瘤免疫逃避有关,可为宫颈癌、食管癌等肿瘤的病因学提供新的线索。     

T cell response in hepatitis C virus infection.

Hepatitis C virus (HCV) is a hepatotropic RNA virus that causes acute and chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma. It is widely accepted that cellular immune responses play an important role in viral clearance and disease pathogenesis. However, HCV often evades effective immune recognition and has a propensity to persist in the majority of acutely infected individuals (ca. 80%). The immunological and virological basis for the inefficiency of the cellular immune response to clear or control the virus is not known. Recent studies, however, have provided new insights into the mechanisms of viral clearance and persistence that will be discussed in detail.     

CD8+T淋巴细胞非细胞毒性抗HIV作用研究进展

细胞免疫在抗病毒感染中发挥着至关重要的作用。人类免疫缺陷病毒(HIV)感染所引起的细胞免疫反应是由CD8 T淋巴细胞的亚群细胞毒性T细胞(CTL)介导的先天免疫。CTLs一方面通过细胞毒性作用杀伤感染的细胞,另一方面分泌可溶性抗病毒因子(CAF)发挥直接的抗病毒作用,因此成为HIV感染中细胞免疫的重要组成部分。本文就HIV感染这一疾病过程中CD8 T淋巴细胞所发挥的非细胞毒性抗病毒效应作一概述。     

Evasion of host immune surveillance by hepatitis C virus: potential roles in viral persistence

Hepatitis C virus (HCV) is a major human pathogen that causes mild to severe liver disease worldwide. This positive strand RNA virus is remarkably efficient at establishing chronic infections. In order for a noncytopathic virus such as HCV to persist, the virus must escape immune recognition or evade host immune surveillance. Immune escape via the hypervariable region of the E2 envelope protein has been postulated as one mechanism for HCV persistent infection. Such hypervariability within the E2 protein may be under selective pressure from protective B cell or T cell responses and be able to escape immune recognition by rapid mutation of antigenic site. In addition to antigenic variation, HCV may also suppress immune response, leading to dampening of cellular immunity. This is supported by recent studies in our laboratory demonstrating that the HCV core protein can suppress host immune responses to vaccinia virus by downregulating viral specific cytotoxic T lymphocyte (CTL) responses and cytokine production. An understanding of the mechanisms behind HCV persistence will provide a basis for the rational design of vaccines and novel therapeutic agents targeting human HCV infection.