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羊口疮是一种人兽共患传染病,主要由羊口疮病毒(Orf virus,OrfV)感染所致,目前尚无特效药物可治疗。囊膜蛋白是OrfV的主要抗原性蛋白,其机理主要是为病毒侵入宿主细胞创造一系列条件,同时降低宿主免疫力,增强了病毒的毒力。当病毒侵入宿主体内后,宿主会产生抗病毒免疫应答来清除病毒粒子,包括特异性体液免疫和非特异性细胞免疫应答,但主要以非特异性的细胞免疫应答为主。宿主对病毒会产生抗病毒免疫应答,同时病毒也会对宿主的免疫应答形成一种免疫逃避机制,通过该机制来躲避宿主免疫细胞对病毒粒子的捕获和清除,为病毒粒子在宿主体内的增殖、成熟及增强病毒毒力创造了各种条件。作者归纳总结了近年来羊口疮病毒与宿主互作的研究,阐述了OrfV囊膜蛋白的生物学功能、宿主的抗病毒免疫应答、病毒在宿主体内的免疫逃避机制和OrfV的其他一些毒力因子的致病作用,以期为羊口疮病毒的致病机制及疫苗防制研究提供参考。 相似文献
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羊口疮(orf)是由羊口疮病毒(orf virus, ORFV)感染引起的一种高度接触性、嗜上皮性人兽共患传染病,不但阻碍畜牧业发展,而且危害人类健康。ORFV感染诱导宿主强烈的免疫反应和炎症反应,但宿主仍可被ORFV反复感染,主要是因为ORFV在与宿主的长期相互作用过程中,发展和进化出多种免疫逃逸机制。ORFV主要通过抑制干扰素反应、抑制NF-κB信号通路、抑制炎症反应、调控细胞凋亡、细胞周期、自噬和血管增生等方式实现免疫逃逸。ORFV免疫逃逸主要是通过其编码的多个免疫调控蛋白来实现。本文主要对ORFV感染引起的宿主免疫应答、ORFV免疫逃逸机制的最新研究进展进行综述,旨在为orf疫苗研制及综合防控提供重要参考。 相似文献
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《中国预防兽医学报》2019,(9)
正在病毒与宿主进化的过程中,E3泛素连接酶作为宿主和病毒联系的桥梁,介导这二者之间的相互作用。在宿主细胞中,E3泛素连接酶通过调节宿主细胞的抗病毒免疫应答间接地抑制病毒复制,如调控信号通路、细胞凋亡和细胞分化等。此外,E3泛素连接酶也可以直接靶向并降解病毒编码蛋白调控病毒复制。为逃逸宿主的抗病毒反应,许多病毒编 相似文献
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新城疫(Newcastle disease)是由新城疫病毒(Newcastle disease virus,NDV)感染大多数禽类,以发生呼吸困难、头冠紫黑和下痢等症状的一种急性、高度接触性传染病。该病一年四季均可发生,但以冬季最为严重,不同曰龄鸡均可感染。被世界动物卫生组织(OIE)列为法定报告的动物疫病之一。对禽类养殖业危害较大。NDV属单股负链RNA病毒目、副黏病毒科、副黏病毒亚科、胳腺炎病毒属的禽副黏病毒。在NDV感染宿主后,病毒可以产生一系列反应以应对宿主的免疫应答以利于自己的病毒复制,起到免疫逃避的作用。NDV免疫逃避机制主要通过抑制与干扰素相关反应、抑制细胞凋亡以及利用宿主真核翻译系统逃逸宿主免疫反应等途径实现。 相似文献
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视黄酸诱导基因Ⅰ(RIG-Ⅰ)为RLRs受体家族的成员,是比较关键的细胞质内病原体识别受体,可识别细胞内的单链、双链等RNA病毒成分,被激活的RIG-Ⅰ受体及其CARD在TRIM25的作用下连接泛素链使其寡聚化,通过与线粒体抗病毒信号蛋白(MAVS)相互作用,激活MAVS及下游转录因子IRF3和NF-κB,从而诱导Ⅰ型干扰素和炎性因子的表达,最终介导宿主的抗病毒免疫应答。鉴于RIG-Ⅰ持续激活可导致炎性因子对自身细胞的损伤,因此RIG-Ⅰ样受体信号通路受到宿主严格的调控。而某些病毒为逃避宿主细胞的免疫应答,进化出多种机制靶向调节RIG-Ⅰ及MAVS,从而阻断信号通路。论文从RIG-Ⅰ识别病毒机制、激活下游信号传导、宿主细胞对信号传导途径的调控以及病毒逃避机制等方面重点阐述RIG-Ⅰ所介导的天然免疫反应。 相似文献
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《畜牧兽医学报》2015,(4)
流感病毒是一种重要的呼吸道疾病病原,在人群中每年都会造成地方性流行,因其抗原性易发生变异,多次引起世界性大流行。流感病毒也可在多种动物群体持续传播,偶尔可经动物感染人类并在人群中传播和适应,一定条件下给人类健康造成潜在的威胁。天然免疫应答,特别是干扰素应答是机体早期抵御病毒感染的关键屏障;病毒突破这道屏障,才能成功感染宿主。为对抗病毒感染,宿主细胞利用一系列精密的抗病毒策略:利用模式识别受体识别病毒表达的产物,激活一系列信号级联反应,并导致干扰素等细胞因子的产生;干扰素诱导下游效应分子的表达,进而抑制病毒复制,并辅助机体引发特异性免疫。在与宿主共进化过程中,流感病毒也形成一套完善的拮抗宿主干扰素通路的策略,使病毒能有效地在宿主细胞中感染和传播。最近几年,关于病毒诱导和调控宿主天然免疫应答的研究取得突飞猛进的发展,特别是大量研究发现病毒可以利用各种策略逃避宿主的抗病毒应答。因此,本综述主要介绍流感病毒如何拮抗宿主的干扰素产生而逃避细胞抗病毒应答,有助于揭示流感病毒的致病机制和发现新的抗病毒靶标,从而为防控流感病毒感染奠定基础。 相似文献
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Sang Y Rowland RR Blecha F 《Animal health research reviews / Conference of Research Workers in Animal Diseases》2011,12(2):149-167
Innate immunity provides frontline antiviral protection and bridges adaptive immunity against virus infections. However, viruses can evade innate immune surveillance potentially causing chronic infections that may lead to pandemic diseases. Porcine reproductive and respiratory syndrome virus (PRRSV) is an example of an animal virus that has developed diverse mechanisms to evade porcine antiviral immune responses. Two decades after its discovery, PRRSV is still one of the most globally devastating viruses threatening the swine industry. In this review, we discuss the molecular and cellular composition of the mammalian innate antiviral immune system with emphasis on the porcine system. In particular, we focus on the interaction between PRRSV and porcine innate immunity at cellular and molecular levels. Strategies for targeting innate immune components and other host metabolic factors to induce ideal anti-PRRSV protection are also discussed. 相似文献
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非洲猪瘟(African swine fever,ASF)是由非洲猪瘟病毒(African swine fever virus,ASFV)感染猪引起的一种急性、烈性、高度接触性传染病,至今没有研发出安全有效的疫苗,一旦暴发会造成重大经济损失。ASFV在和宿主长期作用过程中,通过抑制干扰素和炎症反应,调节凋亡、自噬及细胞免疫等多种途径逃逸机体免疫反应促进自身复制,但具体的机制仍不完全清楚。ASFV复杂的免疫逃逸机制可能是阻碍有效疫苗研发的关键因素之一。借助生物信息学技术对ASFV的基因组和蛋白质组深入分析,筛选病毒的免疫调控关键基因和保护性抗原表位,将在ASFV免疫逃逸分子机制的研究与疫苗研发中发挥重要作用。本文主要对ASFV感染引起的免疫应答反应及可能的免疫逃逸机制研究进行概述,以期为ASF疫苗研制及综合防控提供思路。 相似文献
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Srikumaran S Kelling CL Ambagala A 《Animal health research reviews / Conference of Research Workers in Animal Diseases》2007,8(2):215-229
Bovine respiratory tract disease is a multi-factorial disease complex involving several viruses and bacteria. Viruses that play prominent roles in causing the bovine respiratory disease complex include bovine herpesvirus-1, bovine respiratory syncytial virus, bovine viral diarrhea virus and parinfluenza-3 virus. Bacteria that play prominent roles in this disease complex are Mannheimia haemolytica and Mycoplasma bovis. Other bacteria that infect the bovine respiratory tract of cattle are Histophilus (Haemophilus) somni and Pasteurella multocida. Frequently, severe respiratory tract disease in cattle is associated with concurrent infections of these pathogens. Like other pathogens, the viral and bacterial pathogens of this disease complex have co-evolved with their hosts over millions of years. As much as the hosts have diversified and fine-tuned the components of their immune system, the pathogens have also evolved diverse and sophisticated strategies to evade the host immune responses. These pathogens have developed intricate mechanisms to thwart both the innate and adaptive arms of the immune responses of their hosts. This review presents an overview of the strategies by which the pathogens suppress host immune responses, as well as the strategies by which the pathogens modify themselves or their locations in the host to evade host immune responses. These immune evasion strategies likely contribute to the failure of currently-available vaccines to provide complete protection to cattle against these pathogens. 相似文献
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It is well documented that there is a delay in the development of effective immunity to porcine reproductive and respiratory syndrome virus (PRRSV) in infected and vaccinated pigs. This suggests that PRRSV might possess some inherent properties to evade host defense mechanisms during the early stage of infection. Dendritic cells (DCs) play a crucial role in the activation and control of T-cells in response to viral antigens. In this study, we investigated the phenotypic and functional property changes of bone marrow-derived immature DCs (BM-imDCs) that take place after infection by PRRSV. Results showed that BM-imDCs were permissive to PRRSV infection, as productive replication took place in these cells. A down-regulated expression of MHC I molecules along with an up-regulated expression of CD80/86 is observed at 48 h following infection. Also at 48 h following PRRSV infection, a significant increase of IL-10 secretion by BM-imDCs was noticed. Results suggest that the inhibited expression of MHC I and the enhanced secretion of IL-10 by BM-imDCs after PRRSV infection might be among the strategies used by the virus to evade the host immune defenses. 相似文献
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羊痘病毒免疫学研究进展 总被引:4,自引:2,他引:2
羊痘病毒是在细胞浆中复制的DNA病毒,能引起羊和牛的皮肤病变.病毒编码一系列免疫调节基因和引起宿主细胞凋亡的基因来逃避宿主先天和后天的免疫反应.病毒感染机体后,主要引起宿主的细胞免疫.羊痘病毒能增强机体对其他免疫原的免疫反应. 相似文献
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Parasite defense mechanisms for evasion of host attack; a review 总被引:2,自引:0,他引:2
This review covers some of the basic mechanisms whereby parasites evade host responses. These mechanisms include; antigenic variation, repeated antigenic determinants, induction of suppressor cells, acquisition of host proteins or molecular mimicry, proteinase destruction of host effector molecules, proteinase inhibitor-mediated inhibition of humoral and cellular immune effector arms and immunosuppressive products of parasite arachidonic acid metabolism. Vet. Parasitol. 相似文献
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D C Ruffin 《Veterinary Clinics of North America: Food Animal Practice》2001,17(2):315-32, vi-vii
Mycoplasmas have complex mechanisms of antigenic variation that allow them to evade the immune system. These organisms cause a variety of clinical syndromes that can have a significant economic effect on small ruminant production. The syndromes range from acute septicemia and death to chronic infection resulting in decreased production. Recent research findings have shed light on the means by which these organisms evade the host immune response and cause or contribute to the development of disease in the host. This article provides a review of the pathogenesis, clinical signs, and treatment options for common disease syndromes involving Mycoplasma spp. in small ruminants. 相似文献
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Wensman JJ Ilbäck C Hjertström E Blomström AL Gustavsson MH Jäderlund KH Ström-Holst B Belák S Berg AL Berg M 《Veterinary immunology and immunopathology》2011,141(1-2):162-167
Borna disease virus (BDV) is a neurotropic, negative-stranded RNA virus, which causes a non-suppurative meningoencephalomyelitis in a wide range of animals. In cats, BDV infection leads to staggering disease. In spite of a vigorous immune response the virus persists in the central nervous system (CNS) in both experimentally and naturally infected animals. Since the CNS is vulnerable to cytotoxic effects mediated via NK-cells and cytotoxic T-cells, other non-cytolytic mechanisms such as the interferon (IFN) system is favourable for viral clearance. In this study, IFN-γ expression in the brain of cats with clinical signs of staggering disease (N=12) was compared to the expression in cats with no signs of this disease (N=7) by quantitative RT-PCR. The IFN-γ expression was normalised against the expression of three reference genes (HPRT, RPS7, YWHAZ). Cats with staggering disease had significantly higher expression of IFN-γ compared to the control cats (p-value ≤ 0.001). There was no significant difference of the IFN-γ expression in BDV-positive (N=7) and -negative (N=5) cats having clinical signs of staggering disease. However, as BDV-RNA still could be detected, despite an intense IFN-γ expression, BDV needs to have mechanisms to evade this antiviral immune response of the host, to be able to persist. 相似文献
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病原微生物荚膜多糖的生物学功能 总被引:2,自引:1,他引:1
荚膜多糖(capsular polysaccharide,CPS)是一种广泛存在于细菌、支原体、部分真菌等菌体表面的碳水化合物。同时,荚膜多糖有助于菌体抵抗干燥和低温等不利环境,并通过在菌体表面形成物理屏障阻碍宿主补体的杀伤与吞噬作用。在长期多种应激-压力环境下,病原菌已进化出多种免疫逃避机制并促进宿主感染;在非病原微生物中,荚膜多糖可正向调节宿主免疫作用,并拮抗机体免疫因子,保护宿主免受病原菌引起的炎症性疾病。本文将结合本团队的相关研究工作,对荚膜多糖的结构、合成调控机制、生物学功能、免疫逃避机制和致病机制,特别是荚膜多糖正向调节宿主免疫系统及其应用潜力等方面作一综述,为病原菌致病机制的研究和疫病的有效防控提供参考依据。 相似文献