病毒免疫逃逸防卫机制

从各种各样的病毒免疫逃逸机制中归纳概括出病毒逃避宿主抗感染反应的三个大方面,包括病毒逃避体液免疫系统的识别、病毒抑制细胞免疫应答以及病毒干扰免疫效应功能,以期为研制新的病毒疫苗和抗病毒药物提供参考。在宿主和病毒的长期共同进化过程中,宿主发展了各种免疫机制以清除病毒,而病毒则进化出各种免疫逃逸机制来躲避宿主的免疫应答。     

病毒的持续性感染机制研究进展

病毒感染存在急性与持续性两种形式,急性感染有利于病毒在不同宿主间迅速传播。然而,一方面由于宿主具备多种抵御和清除病毒感染机制来抑制病毒的过度增殖,另一方面由于病毒在感染过程与宿主共同进化,在保证自身不被宿主免疫系统清除的同时,又避免与机体免疫系发生正面冲突,这种类似于寄生的持续性感染方式可能更有利于其长久繁衍。病毒可以降低宿主的防御和减轻病毒对机体的损伤,因而许多持续性感染病毒并不杀伤细胞,然而持续性感染的建立并非只是病毒单方面的决定,而是由病毒和宿主等多种因素共同作用的结果。其中与免疫细胞的相互作用是病毒引起持续性感染的重要原因,虽然某些机制目前还未完全清楚,但存在一些共同的机制。本文针对持续性感染病毒与免疫细胞之间相互作用的研究进展作一综述。     

内源性绵羊肺腺瘤病毒与宿主共进化研究进展

近年来的研究表明,内源性逆转录病毒作为哺乳动物基因组的重要组成部分,在与宿主共进化过程中发挥重要作用.对内源性绵羊肺腺瘤病毒的研究,为揭示哺乳动物内源性逆转录病毒与宿主共进化关系提供了一个独特的模型系统.内源性绵羊肺腺瘤病毒在与宿主共进化过程中不断的增强自身的宿主适应性,通过取代宿主原有的促进孕体发育及胎盘形成的机制而...     

禽类病毒免疫逃避的机制

为了在宿主体内生存,病毒在进化过程中形成了一系列逃避机体免疫的能力,包括潜伏感染、抗原变异、干扰抗原加工和呈递、调节宿主细胞因子网络、调控细胞凋亡以及抑制补体抗体系统等.本文以禽病毒为例对病毒免疫逃避的机制进行了综述.     

病毒感染细胞过程中caspases介导的病毒蛋白自剪切研究概况

很多宿主细胞在病毒感染下通常会启动caspases通路凋亡途径导致细胞死亡,避免病毒的进一步扩增和传播.但最近的一些研究表明,病毒能利用激活的caspase蛋白酶对自身(非)结构蛋白进行特异性剪切,以利于病毒在细胞内的复制或参与病毒或宿主其他基因的转录调控等过程.作为一个病毒与宿主细胞相互作用关系的新的研究领域,论文对...     

流感病毒种内与种间传播的影响因素

A型流感病毒具有相对的宿主特异性,病毒在种内和种间的传播案例经常发生.对于某一特定宿主,病毒的感染受到诸多因素影响,包括病毒、宿主和环境因素等.本文对影响流感病毒种内和种间传播的因素进行概述.     

RIG-Ⅰ样受体信号传导通路与调控机制研究进展

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。     

禽流感病毒的传播及流行进化特点

禽流感病毒,尤其是高致病性禽流感病毒是一种可以引起人兽共患病的病原,由其引发的禽流感疫情不仅给养禽业带来了严重打击,而且也给人类健康和生命安全带来了严重威胁。尽管目前还未发生人际传播,但该病毒一旦与人流感病毒重组,将会转变为可人间传播的高致死性流感病毒,从而导致新的流感大流行。文章综述了近年来禽流感病毒的传播机制、血凝素和聚合酶与禽流感病毒跨宿主传播的关系、禽流感病毒的流行与进化特点等国内外研究成果,为禽流感的科学防控提供技术依据。     

犬流感病毒的研究进展

犬流感(CI)是由犬流感病毒(CIV)引起的以呼吸道症状为主的犬类传染性疾病。2004年,在犬体内发现马源犬流感病毒后,人源、猪源、禽源等多种不同动物来源的犬流感病毒相继出现。这些病毒在犬体内复制、重配,甚至通过犬传播至其他宿主,对其他动物造成威胁。文章以犬流感的进化过程为基础,分析流感病毒在宿主改变过程中发生的对犬的适应性变化,以及不同犬流感的重点防治方向。     

流感病毒受体结合与抗原性改变的分子基础

流感病毒的血凝素(HA)与宿主细胞表面糖链末端唾液酸(SA)的结合对流感病毒感染宿主起着至关重要的作用。禽流感病毒对SAα2-3Galβ糖链以及人流感病毒对SAα2-6Galβ糖链的结合特异性使跨种属传播受阻,但不同的流感病毒在猪和陆地家禽等中间宿主体内发生基因重配作用后,可使部分禽流感病毒获得适应性感染人的能力,另一方面,流感病毒自身的基因突变,尤其是受体结合部位周围的特定位点,可导致流感病毒受体结合特异性发生转变,而病毒的变异伴随着自身糖修饰和抗原表位的改变,使机体对其免疫识别结合的能力也随之发生变化。这些分子水平的改变都将对病毒相关的宿主受体结合和免疫应答反应产生影响。     

Mechanisms of survival of nematode parasites with emphasis on hypobiosis

Mechanisms involved in parasitic nematode survival must be considered with reference to their host and environmental interrelationships since these interrelationhips ultimately influence any parasite adaptations aimed at survival.The most important of the potential environmental constraints are climatic, particularly temperature and humidity, and these can drastically influence larval development and survival.One of the major host factors influencing successful parasite survival is the availability of suitable (susceptible) new hosts to the infective stages of the parasite at the appropriate time for transmission to be achieved. Other host factors that influence parasite survival are those that affect the entrance, establishment and reproduction of the parasite within its new host; mainly problems of acclimatization to a parasitic way of life as well as the countering or adaptation to a variety of host resistance factors, both molecular and cellular, by the parasite.Finally in order for life cycles to be completed, the parasite must evolve means whereby its larval forms can leave the host so that eventual transmission to a new host can be accomplished.In this paper a number of adaptations which enable the parasite to overcome these constraints are discussed. These include such things as larval resistance to environmental effects, the utilization of intermediate hosts or vectors for transmission, seasonally-increased fecundity rates, anti-host immunity stratagems and hypobiosis.This latter phenomenon, hypobiosis or prolonged but temporarily arrested larval development, represents one of the most useful of life cycle adaptations to ensure parasite adaption enables the parasite to synchronize its life cycle to changing environmental or survival and appears to be widespread among parasitic nematodes. Among its benefits, this host conditions. It can thus be of major importance in ensuring survival of the parasite during periods of environmental adversity when conditions for transmission are poor and survival of free-living forms may be minimal. It also enables the parasite to have available large numbers of infective forms at points in the host reproductive cycle which coincide with the production of the susceptible neonates thereby greatly facilitating transmission. Additionally, with certain species of nematodes, occurring as it does at times of the year when the numbers of infective stages may be high while host resources may be limited, oscillations in parasite biomass can be avoided. It thus serves as a highly adaptive mechanism for regulating populations of adult worms, lessening stress on the host and favoring parasite survival as a result.     

血吸虫的抗原伪装研究进展

抗原伪装是包括寄生虫在内的病原体的一种逃避宿主免疫反应方式.血吸虫在宿主间的转移实验证明了血吸虫具有抗原伪装现象.在血吸虫生活史的主要阶段均发现了许多与宿主相同的抗原以及众多的免疫抑制物质.这些物质有些是血吸虫自身表达的,有些是血吸虫结合的宿主抗原.它们通过掩盖血吸虫抗原等多种机理伪装血吸虫进而使血吸虫逃避宿主的免疫攻击.     

White spot syndrome virus: an overview on an emergent concern

Viruses are ubiquitous and extremely abundant in the marine environment. One of such marine viruses, the white spot syndrome virus (WSSV), has emerged globally as one of the most prevalent, widespread and lethal for shrimp populations. However, at present there is no treatment available to interfere with the unrestrained occurrence and spread of the disease. The recent progress in molecular biology techniques has made it possible to obtain information on the factors, mechanisms and strategies used by this virus to infect and replicate in susceptible host cells. Yet, further research is still required to fully understand the basic nature of WSSV, its exact life cycle and mode of infection. This information will expand our knowledge and may contribute to developing effective prophylactic or therapeutic measures. This review provides a state-of-the-art overview of the topic, and emphasizes the current progress and future direction for the development of WSSV control strategies.     

Zoonotic aspects of arenavirus infections

To date, the International Committee for Taxonomy of Viruses recognizes that the family Arenaviridae contains a unique genus Arenavirus that includes 22 viral species. There are nine additional arenaviruses that either have been discovered recently, or which taxonomic status remains pending. Arenaviruses have been classified according to their antigenic properties into two groups, the Lassa-Lymphocytic choriomeningitis (LCM) serocomplex and the Tacaribe serocomplex which has been further divided into four evolutionary lineages. Each arenavirus is more or less tightly associated with a mammal host. The distribution of the host dictates the distribution of the virus. Humans may become infected by arenaviruses through direct contact with infected rodents, including bites, or through inhalation of infectious rodent excreta and secreta. Lassa, Junin, Machupo, Guanarito, and Sabia viruses are known to cause a severe hemorrhagic fever, in western Africa, Argentina, Bolivia, Venezuela, and Brazil, respectively. Infection by LCM virus can result in acute central nervous system disease, congenital malformations, and infection in organ transplantation recipients. Detection of arenaviruses in their animal host can be achieved by virus isolation, and has recently taken advantage of PCR-based techniques. The approach based on consensus degenerate primers has shown efficient for both detection of known arenaviruses, and discovery of new arenaviruses.     

Gorillas are a host for Dientamoeba fragilis: an update on the life cycle and host distribution

Dientamoeba fragilis is a gastrointestinal protozoan that has a worldwide distribution and is emergeing as a common cause of diarrhea. As D. fragilis has a propensity to cause chronic illness with symptoms similar to irritable bowel syndrome (IBS) it is not surprising that some patients with D. fragilis are misdiagnosed as having IBS. In contrast to most other pathogenic protozoa very little is known about its life cycle, epidemiology and mode of transmission. What role animal reservoirs play in the transmission of this parasite is unknown. Consequently we undertook a prospective study to determine the host distribution of D. fragilis. Over a 2-year-period, 608 faecal samples from a wide range of animal and bird species, including pigs and other food species, were screened using permanent stained smears for the presence of D. fragilis. Trophozoites of D. fragilis were only detected in Western lowland gorillas (3/10) (Gorilla g. gorilla) and confirmed by PCR targeting the SSU rRNA gene. The limited host range detected suggests human infection may not involve transmission from other animal species. In addition, we provide an update on the limited knowledge about the life cycle of this parasite and its host distribution.     

High within-host genetic variation of the nematode Spirocerca lupi in a high-density urban dog population

The nematode worm Spirocerca lupi has a cosmopolitan distribution and can cause the death of its final canid host, typically dogs. While its life cycle, which involves a coprophagous beetle intermediate host, a number of non-obligatory vertebrate paratenic hosts and a canid final host, is well understood, surprisingly little is known about its transmission dynamics and population genetic structure. Here we sequenced cox1 to quantify genetic variation and the factors that limit gene flow in a 300 km(2) area in South Africa. Three quarters of the genetic variation, was explained by differences between worms from the same host, whereas a quarter of the variation was explained by differences between worms from different hosts. With the help of a newly derived model we conclude that while the offspring from different infrapopulations mixes fairly frequently in new hosts, the level of admixture is not enough to homogenize the parasite populations among dogs. Small infrapopulation sizes along with clumped transmission may also result in members of infrapopulations being closely related.     

A novel epidemiological model to better understand and predict the observed seasonal spread of Pestivirus in Pyrenean chamois populations

Seasonal variations in individual contacts give rise to a complex interplay between host demography and pathogen transmission. This is particularly true for wild populations, which highly depend on their natural habitat. These seasonal cycles induce variations in pathogen transmission. The seasonality of these biological processes should therefore be considered to better represent and predict pathogen spread. In this study, we sought to better understand how the seasonality of both the demography and social contacts of a mountain ungulate population impacts the spread of a pestivirus within, and the dynamics of, this population. We propose a mathematical model to represent this complex biological system. The pestivirus can be transmitted both horizontally through direct contact and vertically in utero. Vertical transmission leads to abortion or to the birth of persistently infected animals with a short life expectancy. Horizontal transmission involves a complex dynamics because of seasonal variations in contact among sexes and age classes. We performed a sensitivity analysis that identified transmission rates and disease-related mortality as key parameters. We then used data from a long-term demographic and epidemiological survey of the studied population to estimate these mostly unknown epidemiological parameters. Our model adequately represents the system dynamics, observations and model predictions showing similar seasonal patterns. We show that the virus has a significant impact on population dynamics, and that persistently infected animals play a major role in the epidemic dynamics. Modeling the seasonal dynamics allowed us to obtain realistic prediction and to identify key parameters of transmission.

Electronic supplementary material

The online version of this article (doi:10.1186/s13567-015-0218-8) contains supplementary material, which is available to authorized users.     

动物干扰素研究概况

随着我国养殖业的迅猛发展,各种疾病的发生和危害日益加重,特别是病毒性疫病,已成为传染病的主体。对于病毒性疾病的治疗仍然缺乏有效的药物,且大多数尚无效果可靠的疫苗,再加上新发和再发病不断出现,使得病毒病危害尤为突出,急待寻找提高机体免疫、抵抗病毒感染的替代药物。干扰素(IFN)作为一种细胞因子具有广谱抗病毒、抗肿瘤和免疫调节活性,还可以促进机体免疫反应,提高机体抗病毒感染能力,使病毒在机体存活和复制的几率降到最低。目前发现Ⅰ型、Ⅱ型和Ⅲ型3种类型的IFN,利用3种类型的IFN的抗病毒和调节免疫的功能,研究抑制病毒复制的新型生物制剂,成为人们关注和研究的热点,为病毒性疫病,特别是新发或突发的重大疫病防控提供参考。     

Immune evasion by pathogens of bovine respiratory disease complex

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.