禽网状内皮组织增殖病

禽网状内皮组织增殖病 (ＲＥ)是继鸡白血病和马立克氏病之后的另 1种病毒性肿瘤病。指由网状内皮组织增殖病病毒 (ＲＥＶ)群的反转录病毒引起的一群病理综合征。这些综合征包括急性网状细胞肿瘤形成、矮小病综合征和淋巴组织与其他组织形成慢性肿瘤。该病毒不仅能通过接触横向传播 ,还能通过鸡胚垂直传播 ,疫苗的广泛污染己成为重要的传染源。近几年来 ,时有鸡群ＲＥ感染的报道。本病的危害不仅在于因感染所致的生长发育障碍或发病死亡 ,更重要的是免疫抑制而引起的继发感染。1　病原学ＲＥＶ属反转录病毒科禽类Ｃ型反转录病毒属。目前己分…     

正视鸡的肿瘤病

在养禽业迅速发展的同时，鸡的疾病也越来越复杂，其中鸡的肿瘤性疾病几乎在实行规模化养殖的国家都有发生。可引起鸡群发生肿瘤的病毒有3种，即鸡马立克氏病病毒（MDV）、鸡白血病病毒（ALV）和禽网状内皮增生病病毒（REV）。     

禽网状内皮组织增殖病研究进展

对禽网状内皮组织增殖病的发生与分布，病原学，发病机制，流行病学，诊断与防治做一综述。     

禽网状内皮组织增殖病病毒对禽流感疫苗免疫效果的影响

为研究禽网状内皮组织增殖病病毒(REV)对禽流感病毒(AIV)疫苗免疫效果的影响,本研究将1日龄SPF鸡经腹腔感染REV HLJR0901株后,分别于10日龄免疫重组AIV灭活疫苗(H5N1亚型,Re-6)、禽流感-新城疫重组二联活疫苗(r LH5-6)及10日龄和24日龄两次免疫r LH5-6疫苗,并设未感染REV的免疫对照组,于免疫后检测血清HI抗体,并采用H5N1亚型高致病性AIV攻毒。结果显示:实验鸡感染REV后HI抗体滴度均低于相应的未感染REV的免疫对照组。感染REV后,免疫一次Re-6灭活疫苗、r LH5-6活疫苗及两次r LH5-6活疫苗的实验鸡攻毒后的存活率分别为70%、60%及80%,排毒鸡数分别为4/10、4/10及3/10;未感染REV的免疫鸡均不发病、不死亡、不排毒;空白对照组实验鸡攻毒后3 d内全部死亡并且排毒。本研究表明,REV对AIV灭活疫苗和活疫苗均具有明显的免疫抑制作用,加强免疫r LH5-6疫苗可以部分减轻该抑制作用。     

四川地区商品代蛋鸡REV、ALV-J感染情况调查

禽网状内皮增生症病毒(REV)和J亚群禽白血病病毒(ALV-J)是引起免疫抑制疾病中最常见的两种病毒.REV日可诱发慢性肿瘤,ALV-J能造成血瘤、肿瘤.但它们在感染鸡群中更多呈业临床感染,并诱发一些非特异性的并发症或免疫抑制,造成禽流感、新城疫等的免疫失败[1].正是由于其呈亚临床感染,无症状往往被养殖户忽视,引起巨大的经济损失.     

Infections Investigation of ALV and REV in Guangxi Local Poultry Breeds and Sequence Analysis of gp85 Gene of ALV Isolates

In order to investigate the infection status of avian leukosis virus (ALV) and avian reticuloendotheliosis virus (REV) in the major local breeds of Qinzhou,Guangxi,totally 953 samples of egg white,cloaca swab and serum of Ma duck,Shitou goose,Tiejiao-Ma chicken,turkey and pigeon were collected from the representing flocks and detected by the commercial ELISA kits.ALV was isolated for the ALV p27 positive samples by culturing on DF-1 cells,and gp85 gene was sequenced.The results showed that the detections of ALV were negative in the samples except those of Tiejiao-Ma chicken,while REV antibody was found positive in Ma duck,Tiejiao-Ma chicken and turkey.The nucleotide sequences of gp85 gene of two isolates shared 94.5% identity with each other,and shared 86.9% to 94.9% with reference strains.The amino acid sequences of gp85 gene of two isolates shared 91.5% identity with each other,and shared 84.0% to 91.6% with reference strains.There were many variable sites in the hyper variable region hr1 and hr2,and the vr2 and vr3 variable regions were relatively conservative.Phylogenetic tree analysis showed that the two isolates shared the highest homology with SCAU11-XG strain.     

猪链球菌性脑膜炎致病机制相关靶细胞、关键致病因子研究进展及中兽医辨证论治初探

<正>猪链球菌病是由猪链球菌(Streptococcus suis,S.suis)引起的一种急性、热性传染病,被我国农业部列为二类动物疫病[1],脑膜炎则是2型猪链球菌(S.suis serotype 2,SS2)引起的主要病症之一,该病症在猪和人均可发生,症状重剧,死亡率高,后遗症严重[2]。此外,SS2还可引起败血症、心内膜炎,关节炎等其他病症。近年来脑膜炎型猪链球菌病的比例有明显上升趋势[3-4]。对于人类,猪链球菌的威     

Analysis on Differential Expression Genes in Porcine Aortic Vascular Endothelial Cells Induced by Apolipoprotein C Ⅲ

The aim of this study was to investigate the differential expression genes induced by ApoCⅢ,and study the function of ApoCⅢ.Porcine aortic vascular endothelial cells were successfully isolated using enzyme digestion,and then screened the differential expression genes induced by ApoCⅢ using the Solexa high-throughput sequencing technology.The results showed 647 differential expression genes,including 390 up-regulated genes and 257 down-regulated genes.The qRT-PCR results verified that the gene expression results from Solexa sequencing data were reliable.GO and Pathway analysis showed that the function of differential expression genes were related to immune response,cell apoptosis and death.These findings suggested that ApoCⅢ affected the physiological function of porcine aortic endothelial cells by the molecular pathways of inflammation,cell adhesion and apoptosis,which provided a theoretical basis for further understanding the molecular mechanisms of atherosclerosis caused by ApoCⅢ.     

内毒素对肠黏膜微血管内皮细胞内分泌一氧化氮和内皮素的影响

目的是研究内毒素（lipopolysaccharide; LPS）导致肠黏膜微血管内皮细胞损伤的作用机制。将所培养的肠黏膜微血管内皮细胞分为空白对照组和LPS组，每组按时间分为4个亚组：3h、6h、9h、12h。空白对照组加维持培养液，LPS组加1μg/ml LPS培养液，在CO2培养箱内静置培养。结果表明，一氧化氮（NO）分泌明显升高，3h后达到高峰，随后逐渐降低，而内皮素（endothelin; ET）分泌急剧升高，9h后达到高峰，随后又开始逐渐降低，但一直保持在较高的水平。所以引起了NO和ET的升高可能是LPS导致肠黏膜微血管内皮细胞的损伤机制。     

Maternal Antibody Protected Chicks from Growth Retardation and Immunosuppression Induced by Early Reticuloendotheliosis Virus Infection

To determine if the maternal antibody from breeders vaccinated with cell culture-adapted reticuloendotheliosis virus （REV） could protect chicks from early REV infection, one-day-old chicks with or without anti-REV maternal antibodies were inoculated with REV, and then their growth rates and antibody titers to Newcastle disease virus （NDV） and avian influenza virus （AIV）, after vaccination with inactivated vaccines, were compared. This study indicated that REV infection could cause growth retardation and severely inhibit immune reactions to inactivated vaccines against NDV and Avian influenza virus （AIV, H9 and H5） in one-day-old broilers without maternal antibodies specific to REV. Maternal antibody from breeders vaccinated with an attenuated REV vaccine effectively protected REV-challenged birds from growth retardation and immunosuppression on antibody reactions to NDV and AIV vaccines. Four weeks after vaccination, the HI titers to NDV, AIV-H9, and AIV-H5 in maternal antibody positive and negative groups were 3.36 ＋- 2.04 versus 1.58± 1.69 （P〈0.01）, 6.27±3.87 versus 0.71 ± 1.60 （P〈0.01）, and 6.72±3.92 versus 0.54± 1.44 （P〈0.01）. Maternal antibodies from breeders vaccinated with REV vaccine could successfully protect chicks from REV infection and effectively prevent REV-induced growth retardation and immunosuppression in antibody responses to NDV and AIV.