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1.
牛病毒性腹泻病毒致病机制研究进展   总被引:1,自引:0,他引:1  
牛病毒性腹泻(bovine viral diarrhea,BVD)和黏膜病(mucosal disease,MD)均是由牛病毒性腹泻病毒(bovine viral diarrhea virus,BVDV)感染引发的传染病,严重威胁世界养牛业的发展。文章概述了BVDV分型及其分子生物学特征,并从急性感染、经胎盘或子宫感染、持续性感染和黏膜病4个方面总结了近期国内外BVDV致病机制的研究进展。根据序列保守性及是否致细胞病变可将BVDV分为两种基因型和两种生物型,其中,新发现的"HoBi"株归类为瘟病毒属。BVDV基因进化很快,基因组编码4种结构蛋白和8种非结构蛋白,编码蛋白在病毒的复制、翻译及在宿主致病过程中发挥重要作用。BVDV致病机制复杂,急性感染会造成病毒血症、繁殖障碍、免疫抑制等,急性感染牛发生腹泻的原因与BVDV感染胃肠道的肌层、黏膜下层并干扰肠道神经的正常功能相关,非致细胞病变型(NCP)BVDV是造成急性感染的病因。胚胎感染BVDV取决于病毒首次侵袭时胎儿在子宫内的生长阶段。NCP型BVDV具有抑制胎儿体内产生Ⅰ型干扰素的能力,致使该病毒在宿主中得以生存并形成持续性感染牛,当持续性感染牛再次感染与NCP型BVDV高度同源的致细胞病变型(CP)毒株时直接诱发黏膜病。两种生物型的产生是发生持续性感染和黏膜病的重要因素,NCP型可向CP型BVDV进行转化。本综述有助于发现控制BVD-MD传播的新途径,为消灭该病和新型疫苗的研制提供参考。  相似文献   

2.
为深入研究牛场中普遍存在的持续性感染,探讨不同生物型牛病毒性腹泻病毒(bovine viral diarrhea virus,BVDV)转化的分子机制,本试验将致细胞病变型BVDV (CP型BVDV)和非致细胞病变型BVDV (NCP型BVDV)感染MDBK细胞,观察细胞变化,感染后12~72 h期间每间隔12 h收集1次细胞,同时对24、48 h收集的细胞进行转录组学分析。结果显示,不同生物型BVDV感染宿主细胞24 h后,与感染NCP型BVDV的细胞相比,感染CP型BVDV的MDBK细胞中上调差异表达的基因2 849个,下调差异表达的基因3 347个,48 h后,上调差异表达的基因2 933个,下调差异表达的基因2 831个。对差异基因的GO功能分析结果表明,差异基因参与的分子功能主要有催化活性、结合活性、酶调节活性、分子转导活性和蛋白结合转录因子活性等;Pathway显著性富集分析结果显示,差异表达基因主要参与细胞自噬、细胞凋亡、免疫调节因子等相关的信号通路。本试验结果可为进一步揭示病毒致病的分子机制、控制BVDV和研制其候选疫苗奠定基础。  相似文献   

3.
牛病毒性腹泻-黏膜病(Bovine viral diarrhoea virus-Mucosal disease,BVDV-MD)是由黄病毒科、瘟病毒属的牛病毒性腹泻病毒(Bovine viral diarrhea virus,BVDV)引起的一种传染病。临床上以发热、腹泻、黏膜糜烂、流产或产畸型胎儿为主要特征。病毒引起的急性疾病称为牛病毒性腹泻,引起的慢性持续性感染称为黏膜病,该病呈世界性分布。  相似文献   

4.
上海嘉定、崇明地区奶牛病毒性腹泻血清学调查研究   总被引:1,自引:0,他引:1  
正牛病毒性腹泻(Bovine viral diarrhea,BVD),又称牛病毒性腹泻/黏膜病(Bovine viral diarrheamucosal disease,BVD/MD)是由牛病毒性腹泻病毒(Bovine viral diarrhea virus,BVDV)引起的急性、接触性传染病。BVDV除感染牛外,还可感染猪,也会感染鹿、羊、骆驼、兔及其他野生动物,宿主相当广泛。近年来也有人感染BVDV,以及从生物制品中分离出BVDV的报道。病牛临床表现为腹泻,急、慢性黏膜病,持续性感染与免疫耐受,母畜流产、产死胎和畸形胎等。本病世界广泛流行,自1980年李佑民首次报道BVDV  相似文献   

5.
牛病毒性腹泻(bovine viral diarrhea,BVD)作为一种病毒性腹泻黏膜病,给养殖业造成了巨大的经济损失,应用疫苗来防控牛病毒性腹泻病毒(bovine viral diarrhea virus,BVDV)依然是重要的方法。直至目前,我国还没有成熟的BVDV疫苗,本研究主要综述了近几年来国外BVDV疫苗的研究进展,旨在为国内BVDV疫苗的研制及应用提供参考。  相似文献   

6.
牛病毒性腹泻诊断技术   总被引:1,自引:0,他引:1  
牛病毒性腹泻/黏膜病(Bovine viral diarrhea-mucosal disease/mucosal disease,BVD/MD),简称牛病毒性腹泻(BVD)或牛黏膜病(BMD),是以牛发热、黏膜糜烂和溃疡、白细胞减少、腹泻、咳嗽及怀孕母牛流产或产出畸形胎儿为主要特征的一种传染病[1].病原是牛腹泻病毒(Bovine viral diarrhea-mucosal disease virus,BVDV),属于黄病毒科(Flaviridae)瘟病毒属(Pestivirus)的成员.根据它在细胞培养物上的特性,BVDV分为两种生物型:一种为致细胞病变型(CP型),能引起细胞形成空泡,核固缩、溶解和死亡等;另一种为非致细胞病变型(NCP型),此型病毒在细胞中复制不引起细胞病变.两种生物型除了与宿主细胞作用不同外,血清型相同.1946年Olafson等首次报道病毒性腹泻病.1980年,李佑民首先证明我国也有本病存在.自20世纪80年代以来,我国已有15个省、市、自治区查出该病,感染动物包括牛、羊、猪、骆驼、鹿等.王新平等对内蒙古、吉林、宁夏等不同地区的牛、羊、鹿群进行了病原学调查,结果发现牛病毒性腹泻病毒的感染率分别为16.5%~89.0%、14.6%~83.3%、19.6%~44.4%,表明本病在国内某些地区存在严重感染。  相似文献   

7.
正牛病毒性腹泻病是由牛病毒性腹泻病毒(bovine viral diarrhea virus,BVDV)感染引起的,以急慢性黏膜病、持续性感染和免疫抑制为主要特征的传染性疾病[1];该病在世界范围流行,给世界养牛业造成了巨大的经济损失。目前BVDV流行趋势呈明显上升状态,给养牛业的安全生产带来了严重的挑战。1疫病流行对我国养牛业的危害通常将BVDV引起临床急性感染症状的疾病  相似文献   

8.
牛病毒性腹泻病毒研究进展   总被引:1,自引:0,他引:1  
<正>牛病毒性腹泻病毒(bovine viral diarrhoea virus,BVDV)主要引起牛病毒性腹泻-黏膜病,造成免疫耐受、持续性感染及母畜的流产、死胎及畸形胎。该病毒呈世界性分布,并可引起猪、羊、鹿、骆驼  相似文献   

9.
抗CP型、NCP型牛病毒性腹泻病毒高免卵黄抗体的制备   总被引:1,自引:0,他引:1  
本研究采用致细胞病变(cytopathic,CP)型牛病毒性腹泻病毒(bovine viral diarrhea virus,BVDV)标准毒和非致细胞病变(noncytopathic,NCP)型新疆优势毒株免疫产蛋鸡,用改良PEG法提取卵黄抗体(IgY),并对提取的IgY采用SDS-PAGE检测纯度,间接ELISA检测免疫后每隔7 d的抗体效价,并测定所得抗体对NCP型BVDV的中和效价。结果表明,用该法提取的IgY纯度较高;间接ELISA结果证明,经过4次免疫后,抗CP型BVDV的效价达到1∶32000,抗NCP型BVDV的效价达到1∶40000,3个月后再次检测,卵黄抗体效价未见明显下降。最后一次免疫14 d的抗体对NCP型BVDV的中和效价达到1×10-3。  相似文献   

10.
奶牛和黄牛病毒性腹泻-黏膜病血清抗体检测   总被引:1,自引:0,他引:1  
牛病毒性腹泻一黏膜病又称牛病毒性腹泻或黏膜病,是由牛病毒性腹泻病毒(Bovine viral diarrhea virus,BVDV)或黏膜病病毒(Mucosal disease,MDV)引起牛以发热、黏膜糜烂溃疡、白细胞减少、腹泻下痢、免疫耐受与持续性感染、免疫抑制与繁殖障碍为特征的传染病。1946年由Olafson等在美国首次发现。本病在世界各国普遍存在,尤其是养牛业比较发达的地区。1980年李佑民自进口奶牛流产胎儿脾脏中分离到该病毒毒株,证明我国也有本病。  相似文献   

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The prevalence of bovine viral diarrhoea virus (BVDV) biotypes and subgenotypes was determined from 131 BVDV positive samples from a diagnostic laboratory. The majority of the isolates were from Oklahoma; however, other states including Kansas, Texas, and Arkansas were represented. These BVDV samples were from submissions of 76 live animals and 55 necropsy samples. There were 131 BVDV samples represented by 117 noncytopathic (NCP), 11 cytopathic (CP) and 3 cases with mixed NCP and CP biotypes. The NCP isolates were more common (P < 0.05) than the CP and NCP/CP combination. The BVDV samples were segregated into three subgenotypes by differential PCR and sequencing of a viral genomic region, 5'-untranslated region (5'-UTR). There were more BVDV1b subgenotypes 60/131 (45.8%) than BVDV1a, 37/131 (28.2%) or BVDV2a, 34/131 (26.0%) (P < 0.05). The organ system involvement included the major categories such as respiratory, digestive, mixed/multiple organs, abortions, and persistent infections (PI). All three BVDV subgenotypes were found in persistently infected (PI) cattle and respiratory diseases, both major requests for BVDV diagnosis. Only one of the 131 viruses was genetically similar to the strains present in U.S. vaccines.  相似文献   

14.
Bovine viral diarrhea virus (BVDV), a Flaviviridae pestivirus, is arguably one of the most widespread cattle pathogens worldwide. Each of its two genotypes has two biotypes, non-cytopathic (ncp) and cytopathic (cp). Only the ncp biotype of BVDV may establish persistent infection in the fetus when infecting a dam early in gestation, a time point which predates maturity of the adaptive immune system. Such fetuses may develop and be born healthy but remain infected for life. Due to this early initiation of fetal infection and to the expression of interferon antagonistic proteins, persistently infected (PI) animals remain immunotolerant to the infecting viral strain. Although only accounting for some 1% of all animals in regions where BVDV is endemic, PI animals ensure the viral persistence in the host population. These animals may, however, develop the fatal mucosal disease, which is characterized by widespread lesions in the gastrointestinal tract. Cp BVD virus, in addition to the persisting ncp biotype, can be isolated from such animals. The cp viruses are characterized by unrestrained genome replication, and their emergence from the persisting ncp ones is due to mutations that are unique in each virus analyzed. They include recombinations with host cell mRNA, gene translocations and duplications, and point mutations. Cytopathic BVD viruses fail to establish chains of infection and are unable to cause persistent infection. Hence, these viruses illustrate a case of “viral emergence to extinction” – irrelevant for BVDV evolution, but fatal for the PI host.  相似文献   

15.
The specificity of the humoral IgG response of cattle naturally or experimentally infected with bovine viral diarrhea virus (BVDV) was studied by radioimmunoprecipitation. Serum samples were tested against radiolabeled lysates of cells infected with cytopathic and noncytopathic biotypes of BVDV. A biotype-specific serologic marker was not detected. The specificity of the IgG induced in cows naturally or experimentally infected with either BVDV biotype was essentially the same. A strong IgG response to the 2 glycoproteins (56 to 58 kilodaltons, [kD] and 48 kD) of both biotypes and to the major polypeptides was induced in infected cells: 118 kD and 80 kD by cytopathic BVDV and only 118 kD by noncytopathic BVDV. The most consistent difference among cattle was the presence of IgG specific for the 37-kD polypeptide. Sequential serum sample collection after spontaneous and induced infections with either BVDV biotype did not indicate specific IgG markers for determining infection history. Sera from cattle with a confirmed diagnosis of mucosal disease and lacking neutralizing antibodies to BVDV usually lacked (greater than 80%) nonneutralizing BVDV-specific IgG. One animal had substantial amounts of IgG to the 80-kD polypeptide. Other cattle had less readily detectable amounts of IgG specific for 80-kD or 37-kD viral polypeptides.  相似文献   

16.
The objective of this study was to verify whether a mixed infection in calves with bovine viral diarrhea virus (BVDV) and other bovine viruses, such as bovid herpesvirus-4 (BHV-4), parainfluenza-3 (PI-3) and infectious bovine rhinotracheitis (IBR) virus, would influence the pathogenesis of the BVDV infection sufficiently to result in the typical form of mucosal disease being produced.

Accordingly, two experiments were undertaken. In one experiment calves were first infected with BVDV and subsequently with BHV-4 and IBR virus, respectively. The second experiment consisted in a simultaneous infection of calves with BVDV and PI-3 virus or BVDV and IBR virus.

From the first experiment it seems that BVDV infection can be reactivated in calves by BHV-4 and IBR virus. Evidence of this is that BVDV, at least the cytopathic (CP) strain, was recovered from calves following superinfection. Moreover, following such superinfection the calves showed signs which could most likely be ascribed to the pathogenetic activity of BVDV. Superinfection, especially by IBR virus, created a more severe clinical response in calves that were initially infected with CP BVDV, than in those previously given the non-cytopathic (NCP) biotype of the virus. Simultaneous infection with PI-3 virus did not seem to modify to any significant extent the pathogenesis of the experimentally induced BVDV infection whereas a severe clinical response was observed in calves when simultaneous infection was made with BVDV and IBR virus.  相似文献   


17.
Based on their action in cell culture, two biotypes of bovine viral diarrhoea virus (BVDV) can be distinguished. The noncytopathic (ncp) BVDV isolated from persistently infected animals cause no visible damage to cultured bovine cells. In contrast, cytopathic (cp) BVDV induces severe damage and apoptosis in cell cultures. Cp BVDV can be isolated from cattle suffering from mucosal disease (MD) and is associated with the severe lesions that primarily affect the gastrointestinal tract. To get an insight into the molecular events during BVDV induced cytopathic effect (CPE), the effect of three chemical reagents (3-aminobenzamide, ascorbic acid and N-acetyl-leucyl-leucyl-methional) with completely different mode of actions in infected cells was analysed. All three substances were able to delay the cytopathic effect induced in permissive bovine cells.  相似文献   

18.
OBJECTIVE: To examine the role of bovine viral diarrhea virus (BVDV) biotype on the establishment of fetal infection in cattle. ANIMALS: 30 mixed-breed pregnant cows. PROCEDURE: Pregnant cows were inoculated oronasally with either i-WNADL, originating from an infectious BVDV cDNA clone of the National Animal Disease Laboratory (NADL) isolate, or the parental virus stock, termed NADL-A. RESULTS: All cows developed neutralizing antibodies to BVDV, and virus was commonly isolated from peripheral blood mononuclear cells or nasal swab specimens of NADL-A inoculated cows; however, virus was rarely isolated from specimens of i-WNADL inoculated cows. i-WNADL did not cause fetal infection, whereas all fetuses harvested from NADL-A inoculated cows at 6 weeks after inoculation had evidence of infection. Immunoblot analysis of fetal virus isolates revealed the absence of NS3, confirming a noncytopathic (NCP) biotype BVDV in the NADL-A stock. The sequence of the NCP contaminant (termed NADL-1102) and the i-WNADL genome were virtually identical, with the exception of a 270 nucleotide-long insert in the i-WNADL genome. Phylogenetic analyses revealed that NADL-1102 forms a monophyletic group with 6 other NADL genomes. CONCLUSIONS AND CLINICAL RELEVANCE: These data suggest that the contaminating NCP virus in the NADL-A stock was the ancestral NADL virus, which originally infected a bovine fetus and recombined to produce a cytopathic (CP) variant. Following oronasal infection of pregnant cows, viremia and transplacental transmission of CP BVDV to the fetus is rare, compared with the high occurrence of maternal viremia and fetal infection observed with NCP BVDV.  相似文献   

19.
Fourteen clinically healthy cattle that were persistently infected with non-cytopathic bovine virus diarrhoea virus (BVDV) and three BVDV-free cattle were inoculated with one of three cytopathic BVDV strains. Mucosal disease developed in 12 of the viraemic cattle, resulting in a moribund condition 17 to 99 days after inoculation. Two of the viraemic cattle remained clinically healthy until the end of the experiment, 14 months after inoculation. The BVDV-free cattle did not develop clinical signs after inoculation. From each cow with mucosal disease a noncytopathic and a cytopathic BVDV strain were isolated from tissue specimens collected post mortem. All the cattle developed moderate to high levels of neutralising antibodies against the cytopathic BVDV strain with which they were inoculated. The antibodies from 10 of the 12 cattle with mucosal disease did not react with the cytopathic BVDV strains isolated post mortem, and antibodies from none of them reacted with the non-cytopathic BVDV isolates. Antibody responses to the inoculated BVDV strains developed earlier in the viraemic cattle than in the BVDV-free cattle.  相似文献   

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