非洲猪瘟病毒的免疫逃逸策略

非洲猪瘟(African swine fever,ASF)是由非洲猪瘟病毒(African swine fever virus,ASFV)引起的一种猪烈性传染病.目前无商品化的ASF疫苗,一旦发病,仅能依靠快速扑杀进行防控,严重威胁我国养猪及相关行业的健康发展.ASF疫苗研发面临的主要困难是对ASFV的毒力相关基因、致...     

非洲猪瘟病毒多基因家族研究进展

非洲猪瘟(African swine fever,ASF)是由非洲猪瘟病毒(African swine fever virus,ASFV)感染引起的一种急性、热性、高度接触性、致死性动物传染病.由于ASFV基因组庞大,变异能力强,免疫逃逸机制复杂,至今无有效药物和疫苗.近年来,对多基因家族的研究取得了很大的进展,可变区多基因家族拷贝数变化是导致ASFV变异的主要原因,且陆续发现多基因家族在决定细胞宿主范围、影响病毒毒力强弱、抑制Ⅰ型干扰素信号通路、抑制干扰素抗病毒效应和促进病毒蜱源感染中具有重要作用.本文对当前的ASFV多基因家族研究进展进行总结,阐述其在基因变异和病毒感染中的作用,以期为非洲猪瘟免疫逃逸机制的探索和疫苗的研发提供理论依据.     

非洲猪瘟病毒的生物学特性与疫苗研制的难点

非洲猪瘟(African swine fever,ASF)是由非洲猪瘟病毒(African swine fever virus,ASFV)引起的一种猪烈性传染病,是全球养猪业的"头号杀手",强毒株引发的超急性和急性感染死率高达100%。2018年8月ASF首次传入我国,截止2019年6月6日,已有32个省份累计暴发137起疫情,给我国社会、经济构成巨大威胁。ASF疫苗的研制始于20世纪60年代,但均以失败而告终,其主要原因是对ASFV生物学特性缺乏深入的研究。有效控制当前ASF疫情扩散、研制安全有效的疫苗将是我国面临的巨大挑战。本文对ASFV形态与基本结构、传播途径、致病机制、基因组及编码蛋白、入侵机制、免疫逃逸等生物学特性进行了概述,并分析了当前疫苗研制面临的难点,以期为我国有效控制ASF疫情及病原研究提供参考。     

非洲猪瘟病毒跨膜蛋白CD2v的结构与功能研究进展

非洲猪瘟(African swine fever,ASF)是由非洲猪瘟病毒(African swine fever virus,ASF V)感染家猪和野猪,引起的高度传染性和致死性动物传染病,不同品种和年龄阶段的猪均易感,发病率和死亡率可高达100％.ASFV是全球生猪产业的重点疫病之一,目前无商品化疫苗.ASFV是一种大而复杂的双链DNA双层囊膜病毒.ASFV主要跨膜蛋白CD2v是介导血细胞吸附(Hemadsorption,HAD)和鉴定病毒血清型的关键蛋白,它参与ASFV宿主免疫应答、免疫逃逸和病毒复制等生理生化过程,且是ASFV疫苗和抗病毒分子研发的潜在重要靶点.探究CD2v在ASFV感染中的作用及机制渐成热点.因此,本文对ASFV CD2v的结构及其生物学功能研究报道进行分析综述,将为阐明ASFV致病机理和疫苗研发等提供重要参考.     

非洲猪瘟病毒的非必需基因：真的可有可无吗？

非洲猪瘟（African swine fever,ASF）是由非洲猪瘟病毒（African swine fever virus,ASFV）引起的一种出血性、致死性的猪烈性传染病。ASF在全球广泛传播,给养猪业造成重大的经济损失。ASFV基因组庞大,可编码150多种蛋白,一些非必需基因编码的蛋白与调控病毒毒力、复制和免疫逃逸等相关。通过删除ASFV毒力相关的非必需基因所构建的减毒株是当前比较有前景的疫苗,然而其安全性有待提高。系统地鉴定ASFV非必需基因及其功能,不仅有助于ASF基因缺失疫苗的研发,也有益于ASFV致病机制研究。本文对目前已鉴定的ASFV非必需基因及其功能研究进行了总结分析,着重讨论了影响ASFV毒力、调控病毒复制、参与免疫逃逸的非必需基因及其编码蛋白的功能,旨在加深对ASFV病原学的认识,为新的ASFV非必需基因的鉴定和功能研究提供参考。     

非洲猪瘟病毒调控宿主细胞因子表达水平的研究进展

非洲猪瘟(African swine fever,ASF)是由非洲猪瘟病毒(African swine fever virus,ASFV)引起的一种猪的急性、热性、高度接触性传染病,给全球养猪业造成了巨大的经济损失.ASFV基因组庞大,结构复杂,至今无有效药物和疫苗,只能依靠生物安全对其防控.由于非洲猪瘟发病急的特点,发病后极易引发细胞因子风暴,加快病情发展.本文综述了当前已证实的猪感染ASFV后白介素、干扰素、肿瘤坏死因子等细胞因子的变化及其调控机制.了解细胞因子与ASFV感染的关系,以期对保护性免疫机制的探究奠定基础,为ASFV疫苗研发提供参考.     

我国非洲猪瘟病毒检测技术专利分析

非洲猪瘟（African swine fever, ASF）是由非洲猪瘟病毒（African swine fever virus, ASFV）引起猪的烈性传染病。2018年8月我国首次暴发ASF疫情，由于没有有效的商品化疫苗，导致疫情蔓延至我国各省份。随着疫情的发展，准确、快速的诊断技术成为疫情防控的关键。本文梳理总结了我国ASFV诊断检测技术专利现状，包括ELISA、免疫层析技术等免疫学检测方法和PCR、等温扩增技术、基于CRISPR/Cas系统开发的多种分子生物学检测方法，以期为我国ASF疫病防控及诊断产品的研发提供有价值的参考。     

非洲猪瘟病毒编码蛋白功能研究进展

非洲猪瘟(African swine fever,ASF)是非洲猪瘟病毒(African swine fever virus,ASFV)感染家猪或野猪引起的一种急性、出血性、高度接触性传染病,其特征是病程短、高热和出血性病变,急性感染死亡率高达100%,严重威胁全球养猪业但目前尚未开发出有效的疫苗和治疗方法。ASFV是非洲猪瘟病毒科非洲猪瘟病毒属的唯一成员,为大型双链DNA病毒,主要在巨噬细胞胞质中复制,其基因组约170?193 kb,含有150?167个开放阅读框,编码150?200种蛋白质。目前已知功能的病毒编码蛋白约有50个,大部分为病毒的结构蛋白,仍有一半以上的ASFV编码蛋白功能尚不清楚。除结构蛋白以外,病毒含有完整的酶和与病毒转录有关的因子,编码调节宿主细胞功能及与病毒免疫逃逸相关的蛋白等。本文综述了ASFV的结构蛋白、非结构蛋白以及参与免疫逃逸等相关蛋白功能的研究进展,以期为ASFV病毒蛋白研究及疫苗研发提供相关借鉴。     

非洲猪瘟病毒多样性

非洲猪瘟(African swine fever,ASF)是由非洲猪瘟病毒(African swine fever virus,ASFV)引起猪的一种急性、高度致死性传染病.该病在全世界多个地方流行,导致该病流行的原因之一是缺乏有效的预防及治疗药物、疫苗等.尽管ASFV基因总的突变率相对其基因组来说较低,但是,与其它病毒相比,其基因突变总数则相当巨大.研究发现ASFV的多个基因具有高突变率的特性,表现为基因多样性,此外,由于该病毒为核质大DNA病毒,编码大量蛋白,其抗原也表现为多样性.本文总结了 ASFV基因多样性和抗原多样性,分析其发生原理并综述了最新研究成果,以期为研究ASFV病毒遗传演化、开发疫苗及指导疫情防控提供思路.     

抗非洲猪瘟病毒药物靶点及抗病毒活性物质研究进展

非洲猪瘟（African swine fever,ASF）是由非洲猪瘟病毒（African swine fever virus,ASFV）感染引起的具有高度传染性和致死性的猪烈性传染病。至今尚无有效疫苗和治疗药物可用于ASF防控。2018年ASF首次传入我国,几乎席卷了全国所有省份和地区,给我国养猪业造成了巨大经济损失。目前,ASF在世界上多国蔓延且呈现愈演愈烈趋势,导致ASF疫情在我国反弹的风险极大。在ASF疫苗尚未攻克前提下,研制安全有效的抗ASFV药物对疫情防控具有重要意义。本文通过综述抗ASFV药物作用潜在靶点及抗病毒活性物质研究进展,提出靶向ASFV的pS273R酶、Topo II酶、E165R酶、DNA连接酶、p72和pA104R分子以及靶向细胞微管是最有前景的抗ASFV作用靶点,而金雀异黄素、芹菜素、芫花素和杨梅黄酮等黄酮类成分以及多酚类和多糖类物质具有抗ASFV潜力;同时,通过分析目前抗ASFV药物研究存在的问题（尚未经过体内试验验证）进而指出今后需加强的方向（抗ASFV药物临床研究）,以期为抗ASFV新药研制提供参考。     

Recent advances in the study of Kaposi's sarcoma-associated herpesvirus replication and pathogenesis

It has now been over twenty years since a novel herpesviral genome was identified in Kaposi's sarcoma biopsies. Since then, the cumulative research effort by molecular biologists, virologists, clinicians, and epidemiologists alike has led to the extensive characterization of this tumor virus, Kaposi's sarcoma-associated herpesvirus(KSHV; also known as human herpesvirus 8(HHV-8)), and its associated diseases. Here we review the current knowledge of KSHV biology and pathogenesis, with a particular emphasis on new and exciting advances in the field of epigenetics. We also discuss the development and practicality of various cell culture and animal model systems to study KSHV replication and pathogenesis.     

The structure, reproduction and taxonomy of Vidalia and Osmundaria (Rhodophyta, Rhodomelaceae)

Comprises species occurring mostly in subtidal habitats in tropical, subtropical and warm-temperate areas of the world. An analysis of the type species, V. spiralis (Sonder) Lamouroux ex J. Agardh, a species from Australia, establishes basic characters for distinguishing species in the genus. These characters are (1) branching patterns of thalli, (2) flat blades that may be spiralled on their axis, (3) width of the blade, (4) primary or secondary derivation of sterile and fertile branchlets and (5) position of sterile and fertile branchlets on the thalli. Application of the latter two characters provides an important basic method for separation of species into three major groups. Osmundaria , a genus known only in southern Australia, was studied in relation to Vidalia , and its separation from the Vidalia assemblage is not accepted. Species of Vidalia therefore are transferred to the older genus name, Osmundaria. Two new species, Osmundaria papenfussii and Osmundaria oliveae are described from Natal. Confusion in the usage of the epithet, Vidalia fimbriala Brown ex Turner has been clarified, and Vidalia gregaria Falkenberg, described as an epiphyte on Osmundaria pro/ifera Lamouroux, is revealed to be young branches of the host, Osmundaria prolifera.     

New or rare chromosome counts in Artemisia L. (Asteraceae, Anthemideae) and related genera from Kazakhstan

Fifteen chromosome counts of six Artemisia taxa and one species of each of the genera Brachanthemum, Hippolytia, Kaschgaria, Lepidolopsis and Turaniphytum are reported from Kazakhstan. Three of them are new reports, two are not consistent with previous counts and the remainder are confirmations of very scarce (one to four) earlier records. All the populations studied have the same basic chromosome number, x = 9, with ploidy levels ranging from 2x to 6x. Some correlations between ploidy level, morphological characters and distribution are noted.     

肝癌中HBV和HCV基因和抗原的分布及意义

采用原位分子杂交方法检测HCV RNA及HBV X基因;采用免疫组织化学方法研究HCV核心抗原,非结构区C33c抗原及HBxAg在肝细胞肝癌中的定位及分布.结果表明(1)HCV RNA、HBV X基因在肝细胞肝癌组织检出率分别为40%(55/136)和82%(112/136).HCV RNA定位于癌细胞的胞浆内,阳性细胞呈散在、灶状及弥漫分布三种形式;HBV X基因在肝癌细胞中的分布呈胞浆型、核型及核浆型,阳性细胞也呈上述三种分布形式;(2)HCV C33c抗原、核心抗原在肝细胞肝癌中的阳性率为81%(133/164)及86%(141/164).C33c抗原定位于癌细胞及肝细胞的胞浆内;核心抗原既定位于癌细胞核中,又可定位于胞浆中.C33c抗原阳性细胞以灶状分布为主;而核心抗原阳性细     

Selection with two alleles and complete dominance

For a plant selection model with frequency-independent viabilities, fertilities and selfing rates, it is shown that apart from global fixation, for certain parameter combinations a protected polymorphism and facultative fixation (either allele may become fixed according to initial frequencies) may both occur. Facultative fixation requires different selling rates for the dominant and recessive type. Protection of the polymorphism requires resource allocation for male and female function. In this connection the problem of purely genetically caused population extinction is discussed.
For general frequency dependence and regular segregation, the chances for establishment of a completely recessive gene are compared to those of a completely dominant gene. It is proven that the process of establishment of the recessive gene, despite a fitness advantage, may be considerably endangered by drift effects if random mating prevails. The recessive gene may reach the same effectivity in establishment as a dominant gene, only if the recessive homozygote mates exclusively with its own type during the period of establishment.