猪繁殖与呼吸综合征病毒在我国的流行与进化

猪繁殖与呼吸综合征病毒,引起猪繁殖与呼吸综合征,俗称"猪蓝耳病",是目前持续危害我国养猪业的病原之一。该病毒毒株极具多样性,1995年进入我国后,基因组和致病力不断进化,2006年高致病力毒株引起猪繁殖与呼吸综合征疫情大暴发,造成巨大损失,疫情平息后仍呈地方性流行,时至今日,中低毒力毒株引起的免疫抑制以及高毒力毒株引起的猪只死亡,已是我国猪场面临的巨大难题。对猪繁殖与呼吸综合征病毒在我国的流行与进化进行归纳综述,旨在通过探讨病毒的流行规律,为生产中猪繁殖与呼吸综合征的预防与控制提供参考。     

某猪场猪繁殖与呼吸综合征与猪副嗜血杆菌混合感染

<正>某猪场出现猪繁殖与呼吸综合征与猪副嗜血杆菌疾病混合感染病症。猪繁殖与呼吸综合征(Porcine reproductive and respiratory syndrom PRRS)是由猪繁殖与呼吸综合征病毒     

猪繁殖与呼吸综合征的防制

<正>猪繁殖和呼吸障碍综合征是由猪繁殖与呼吸障碍综合征病毒(PRRSV)引起的猪的一种高度传染性疾病,又称"猪蓝耳病",该病以妊娠母猪的繁殖障碍(流产、死胎、木乃伊胎)及各种年龄猪特别是仔猪的呼吸道疾病为特     

猪蓝耳病诊断与控制

<正>猪蓝耳病又称"猪繁殖与呼吸障碍综合征,是由猪繁殖与呼吸障碍综合征病毒引起的一种高度接触性传染性疾病,由于部分病猪耳部和躯体末端皮肤发绀,故称"蓝耳病"。不同年龄、品种和性别的猪均能感染,但以妊     

关于蓝耳病免疫的是是非非

猪繁殖与呼吸综合征(Porcine Reproductive and Respiratory Syndrome．以下简称：PRRS，蓝耳病)，是一种以引起母猪繁殖障碍和各日龄猪呼吸疾病为特征的接触性传染病，其病原为猪繁殖与呼吸综合征病毒(以下简称PRRSV，蓝耳病病毒)。     

浅谈猪高热综合征的病因与应对措施

就主要发生在生长育成猪和部分母猪、保育猪的高热综合征的病名与内涵进行说明。详细叙述了引起猪高热综合征的诱因,气候与环境、管理与营养、防疫与消毒等应激因素。证明了猪高热综合征是由一种或多种病毒、细菌、支原体、弓形体等混合感染和继发感染,在某些应激因素的诱发下而发生的一种急性传染性疾病。主要病原有猪繁殖与呼吸综合征病毒、猪圆环病毒2型、猪瘟病毒、猪流感病毒、猪伪狂犬病病毒、猪链球菌2型、传染性胸膜肺炎放线菌、副猪嗜血杆菌以及附红细胞体、弓形体、肺炎支原体等。阐明了以猪繁殖与呼吸综合征为主的混合感染、以猪瘟为主的混合感染、以附红体为主的混合感染、以附红体和猪瘟为主的混合感染和以附红体、猪瘟和高致病性猪繁殖与呼吸综合征为主的混合感染的临床症状、剖检病变的特点以及先入为主,误诊错判等诊断误区,提出了应对措施。     

高致病性蓝耳病概述

<正>猪蓝耳病,又称猪的繁殖与呼吸综合征(PRRS),是由动脉炎病毒科中的猪繁殖与呼吸综合征病毒引起的,由国外传入我国,严重影响养猪业的传染病,以繁殖障碍、呼吸困难、耳朵蓝紫、并发其他传染病为主要特征。1987年在美国首先报道了猪繁殖与     

高致病性猪蓝耳病的发病原因及防控对策

<正>高致病性猪蓝耳病(又称猪繁殖与呼吸综合征)是由猪繁殖与呼吸综合征病毒(PRRSV)所引起猪的一种接触性传染病。不同年龄、品种和性别的猪均能感染,但以妊娠母猪和1月龄以内的仔猪更易感染。临诊上以成年猪生殖障碍、早产、流产和死胎,以及仔     

运输引起猪繁殖呼吸障碍综合征的诊治

<正>猪繁殖与呼吸综合征,又称蓝耳病,是由猪繁殖与呼吸综合征病毒引起的一种病毒性传染病,以母猪怀孕后期流产、死产、产弱仔,以及各种年龄段的猪均表现发热、呼吸道症状为     

猪蓝耳病

<正>猪繁殖与呼吸综合征(Porcine reproductive and respiratory syndrome,PRRS),俗称"猪蓝耳病",是由猪繁殖与呼吸综合征病毒(Porcine reproductive and respiratory syndrome virus,PRRSV)引起的以怀孕母猪繁殖障碍和仔猪呼     

Herpesvirus cyprini: a search for viral genome in infected fish by infected fish by in situ hybridization

Abstract. Herpesvirus cyprini (CHV) genome was traced in carp, Cyprinus carpio L., after acute infection by the method of in situ hybridization with biotinylated probes. The viral genome was detected in several tissues including cranial nerve ganglia. Subcutaneous tissue and spinal nerves. However, at this stage, viral antigens were not detected and the virus was not isolated. The viral genome was also detected in the same fish tissues when papillomas were present which contained viral antigens and even infective virus particles. After papilloma regression, the viral genome was still detected in these tissues. It is suggested that CHV becomes latently established in cranial nerve ganglia, subcutaneous tissue and spinal nerves, and is associated with the induction and recurrence of papillomas.     

草鱼出血病病毒854株基因组SDS—PAGE分析及其核酸类型鉴定

十二烷基硫酸钠-聚丙烯酰胺凝胶电泳(SDS-PAGE)结果表明:草鱼出血病病毒854株基因组由11个分段的核酸片段组成,总分子量约为14.46×10~6道尔顿。其中最大片段的分子量约为2.45×10~6道尔顿;最小片段的分子量约为0.38×10~6道尔顿。其基因组核酸片段电泳图谱具有病毒株的特异性.核酸酶敏感性试验表明该病毒的核酸为RNA。     

Betanodavirus: Dissection of the viral life cycle

Progressive research has been recently made in dissecting the molecular biology of Betanodavirus life cycle, the causative pathogen of viral encephalopathy and retinopathy in economic important marine fish species. Establishment of betanodavirus infectious clone allows the manipulation of virus genome for functional genomic study, which elucidates the biological event of the viral life cycle at molecular level. The betanodavirus strategizes its replication by expressing anti‐apoptosis/antinecrotic proteins to maintain the cell viability during early infection. Subsequently utilizes and controls the biological machinery of the infected cells for viral genome replication. Towards the late phase of infection, mass production of capsid protein for virion assembly induces the activation of host apoptosis pathway. It eventually leads to the cell lysis and death, which the lysis of cell contributes to the accomplishment of viral shedding that completes a viral life cycle. The recent efforts to dissect the entire betanodavirus life cycle are currently reviewed.     

Piscine reovirus,but not Jaundice Syndrome,was transmissible to Chinook Salmon,Oncorhynchus tshawytscha (Walbaum), Sockeye Salmon,Oncorhynchus nerka (Walbaum), and Atlantic Salmon,Salmo salar L.

A Jaundice Syndrome occurs sporadically among sea‐pen‐farmed Chinook Salmon in British Columbia, the westernmost province of Canada. Affected salmon are easily identified by a distinctive yellow discolouration of the abdominal and periorbital regions. Through traditional diagnostics, no bacterial or viral agents were cultured from tissues of jaundiced Chinook Salmon; however, piscine reovirus (PRV) was identified via RT‐rPCR in all 10 affected fish sampled. By histopathology, Jaundice Syndrome is an acute to peracute systemic disease, and the time from first clinical signs to death is likely <48 h; renal tubular epithelial cell necrosis is the most consistent lesion. In an infectivity trial, Chinook Salmon, Sockeye Salmon and Atlantic Salmon, intraperitoneally inoculated with a PRV‐positive organ homogenate from jaundiced Chinook Salmon, developed no gross or microscopic evidence of jaundice despite persistence of PRV for the 5‐month holding period. The results from this study demonstrate that the Jaundice Syndrome was not transmissible by injection of material from infected fish and that PRV was not the sole aetiological factor for the condition. Additionally, these findings showed the Pacific coast strain of PRV, while transmissible, was of low pathogenicity for Atlantic Salmon, Chinook Salmon and Sockeye Salmon.     

Propagation of viruses along neuron networks by transsynaptic passage--a contribution to the pathogenesis of rabies

Certain neurotropic viruses are carried along neuronal processes by the axonal transport mechanisms. Indirect morphologic evidence suggests that viral nucleic acid can be transmitted to other neurons by transsynaptic passage. Through this mechanism the viral genome can reach widespread and remote brain areas by propagation along neuronal networks in an intracellular milieu. This type of propagation does not require completion of full replication cycles for cell-to-cell spread; transmission of infective viral nucleic acid is in itself sufficient.     

抗白斑综合征病毒(WSSV)感染途径研究进展

白斑综合征病毒(White Spot Syndrome Virus,WSSV),是引起养殖对虾大规模死亡的病原。在过去的10年中,各国学者不断地寻找预防和控制WSSV感染的方法及途径。本文主要介绍了中和抗体与噬菌体展示单链抗体、免疫增强剂、重组蛋白疫苗和灭活疫苗、遗传育种、RNAi等几种方法的研究现状,为进一步开发抗WSSV药物和饵料,更有效地防治WSSV及相关科研提供参考。     

A simple method for purifying the White Spot Syndrome Virus using ultrafiltration

A very simple and efficient method was developed for isolating intact White Spot Syndrome Virus (WSSV) particles from infected Litopenaeus vannamei tissue. No density gradient centrifugation, ultracentrifugation or protease inhibitors were required for the purification of intact WSSV virions using microfilters (100 kDa cut-off) combined with several steps of conventional centrifugation procedures. A mortality assay was run using healthy shrimp to prove that the virions obtained were infective. The concentrated viral preparations were further studied using polyacrylamide gel electrophoresis (PAGE). At least five distinct protein bands were detected when intact purified WSSV virions were found by sodium dodecyl sulphate-PAGE, followed by Coomassie Brilliant R-250 staining. The estimated molecular weights of these proteins were 23, 24, 29, 32 and 42-kDa, which could correspond to viral protein. Using this method, the virus does not lose its ability to infect healthy shrimp.     

Establishment of a new cell line susceptible to Cyprinid herpesvirus 3 (CyHV‐3) and possible latency of CyHV‐3 by temperature shift in the cells

A new cell line named CCF‐K104 predominantly consisting of fibroblastic cells showed optimal growth at temperatures from 25 °C to 30 °C. Serial morphological changes in the cells induced by Cyprinid herpesvirus 3 (CyHV‐3) included cytoplasmic vacuolar formation, cell rounding and detachment. Mature virions were purified from CyHV‐3‐infected CCF‐K104 cells by sucrose gradient ultracentrifugation and had a typical herpesvirus structure on electron microscopy. Infectious CyHV‐3 was produced stably in CCF‐K104 cells over 30 viral passages. Our findings showed that CCF‐K104 is a useful cell line for isolation and productive replication of CyHV‐3. A temperature shift from 25 °C to 15 °C or 35 °C did not allow serial morphological changes as observed at 25 °C for 14 days. Under the same conditions, real‐time PCR showed that CyHV‐3 was present with low viral DNA loads, suggesting that CyHV‐3 may establish latent infection in CCF‐K104 cells. Amplification of the left and right terminal repeat sequences of the CyHV‐3 genome arranged in a head‐to‐tail manner was detected by nested PCR following an upshift in temperature from 25 °C to 35 °C. The PCR results suggested that the circular genome may represent a latent form of CyHV‐3.     

一株锯缘青蟹呼肠孤病毒的分离纯化及鉴定

在研究锯缘青蟹病害的过程中,从广东某养殖场分离到一株呼肠孤病毒(命名为SsRV)。病毒粒子为球状,直径约45 nm。病毒粒子基因组为12个节段的双链RNA;在1%琼脂糖电泳中SsRV基因组呈1/5/6带型,其分子量分别为3.8,2.5,2.4,2.0,1.9,1.8,1.3,1.2,1.1,1.1,1.0,1.0 kbp。根据病毒的宿主范围、基因组节段数及电泳型,此病毒很可能与地中海滨蟹呼肠孤病毒P和W 2共同构成呼肠孤病毒科一个新的属。