新疆禽白血病感染状况的血清学调查

鸡白血病是由鸡白血病病毒（ALV）引起的一种传染性肿瘤病,感染鸡表现严重生长发育不良等生产性能下降,多组织肿瘤甚至死亡,同时可发生免疫抑制,因此该病一直是种鸡和蛋鸡生产中的重要疫病。近年各地蛋鸡场在鸡群开产后白血病的病例时有发生,给养殖者带来很大经济损失,农业部已经将禽白血病的检测纳入到南方许多省市监测计划中,但在新疆ALV感染问题尚不清楚。     

J亚群禽白血病研究进展

J亚群禽白血病病毒是上世纪90年代初从商品代肉鸡中分离鉴定出来的新的ALV亚群,主要引起肉鸡的骨髓瘤白血病(myloid leucosis,ML)。2009年,J亚群禽白血病在我国呈高发态势。我国于1999年首先在肉用型鸡群分离鉴定出ALV-J的中国株,随后相关研究依次展开。论文就ALV-J的流行病学、检测方法、病毒变异、免疫抑制及与其他免疫抑制疾病共感染等几个方面进行了简要介绍。     

青海省禽白血病血清学调查

正禽白血病(avian leucosis,AL)是由禽白血病病毒(avian leucosis viruses,ALV)引起的一种传染性肿瘤病,感染鸡主要表现为严重的生长发育不良,出现多组织肿瘤甚至死亡,同时可发生免疫抑制。该病的亚临床感染会对鸡群的生产性能产生影响,给养鸡业造成损失。我国将其列为二类动物疫病[1]。禽白血病有A、B、C、D和J等10个亚型,在鸡群中以A、B亚     

IMC10200株ALV-J实验诱发禽骨髓性白血病的研究

对分离自肉种鸡群亚临床感染的J亚群禽白血病病毒IMC1o200株进行了实验感染诱发禽骨髓性白血病的病理学研究.IMC10200株J亚群禽白血病病毒尿囊腔接种11日龄肉鸡胚和SPF蛋鸡胚,孵出后跟踪观察.9周龄时随机抽检感染鸡,感染肉鸡特异引物PCR检测全部为阳性;组织病理学观察感染鸡无明显病变.至21周龄时感染肉鸡出现第一例典型骨髓性白血病病例;感染SPF蛋鸡未见明显J亚群禽白血病相关病变.     

河北省蛋鸡群ALV p27抗原ELISA检测

<正>禽白血病(Avian Leukusis,AL)是由反转录病毒科禽白血病/肉瘤病毒群病毒引起的禽类多种肿瘤性疾病的总称,可引起感染鸡免疫抑制和多组织器官发育迟缓、萎缩以及肿瘤等,造成鸡的生产性能下降甚至死亡,由鸡分离的ALV划分为A、B、C、D、E、J六个亚群。自2002年蛋鸡群发现禽白血病以来,全国各地频发,特别是自2009年以来,湖北、山东等地鸡白血病疑似病例频发,鸡群ALV的感染率高达60%,病死率高达50%以上~([1])。崔治中报道,     

河南地方品种鸡禽白血病病毒感染状况的调查

为了解河南地方品种鸡禽白血病病毒感染状况,2015年10月至2017年4月,在河南地区9个种鸡场,采集了5个河南地方品种1 450只开产母鸡的泄殖腔拭子、血清和蛋清,利用ELISA方法检测3种样品中的禽白血病病毒p27抗原和血清中的禽白血病病毒A/B亚型、J亚型抗体。结果:河南地方品种鸡群总体ALV p27抗原阳性率为泄殖腔拭子22. 62%、血清26. 83%、蛋清12. 90%;鸡群总体血清ALV-A/B亚型、J亚型抗体阳性率分别为24. 76%和19. 52%。5个品种鸡群的血清ALV p27阳性率依次为河南斗鸡84. 48%、淅川乌骨鸡53. 78%、固始鸡19. 81%、三黄鸡17. 22%、卢氏鸡16. 67%,但同品种不同场区间差异较大。表明河南省地方品种鸡群存在不同程度的ALV感染,且可能存在ALV-A/B亚型和ALV-J亚型的同时感染。     

地方特色蛋鸡配套系亲本群中不同亚群禽白血病病毒的混合感染

采用ELISA、病毒分离和多聚酶链式反应(PCR)方法对江苏某地方特色蛋鸡亲本群的禽白血病病毒(ALV)p27抗原、ALV-A/B和ALV-J抗体以及病原核酸进行了检测,结果显示该配套系母本群泄殖腔拭子p27抗原阳性率为40.6%,ALV-A/B抗体阳性率为3.8%;父本群泄殖腔p27抗原阳性率为24.4%,ALV-J抗体阳性率为19.4%;细胞培养物IFA检测显示父本分离株JS12JD03能与J亚群特异单克隆抗体Je-9反应,在荧光显微镜下产生绿色荧光,而母本分离株JS12JD01和JS12JD02则无;gp85氨基酸序列同源性分析显示母本鸡群分离株JS12JD01属于A亚群、JS12JD02属于B亚群,父本鸡群分离株JS12JD03属于J亚群ALV,提示了该地方特色蛋鸡亲本群存在A、B、J亚群ALV的混合感染。     

贵州省地方品种鸡禽白血病病毒流行株的亚型鉴定及其分子特征分析

为了解贵州省9个地方品种鸡群中禽白血病病毒(ALV)流行株亚型与分子特征,本研究2016年从该省8个地区9个地方品种鸡群共采集380份鸡蛋样品。采集卵白用ELISA试剂盒检测ALV-P27抗原,阳性卵白接种CEF和DF1细胞分离病毒,培养7 d后检测细胞培养液中ALV-P27抗原,对感染细胞cDNA以4对ALV特异性引物进行PCR鉴定与分型。并选取9个鸡群的部分ALV分离株进行gp85基因的克隆测序与序列分析。结果表明,9个鸡群的卵白样品ALV-P27抗原阳性率为0~36%;阳性卵白的CEF和DF1细胞培养上清P27抗原检测结果相同,阳性率为26.8%(15/56),并鉴定出其亚型全部为J亚型(ALV-J)。已测序的21株ALV-J gp85基因序列与国内外ALV-J参考株同源性为86.6%~100%;进化树分析显示,21株ALV-J分离株在不同的分支,其进化关系和来源之间未发现明显规律。本研究表明,贵州省9个地方品种鸡群有6个存在ALV-J感染。其中,3个当地培育的品种鸡ALV感染率为0;而来自3个地区的绿壳蛋鸡ALV-P27抗原阳性率普遍较高(26.7%~36.0%)。本研究补充了我国禽白血病流行病学的数据并为该病的防制提供了调查依据。     

广西三黄鸡禽白血病流行病学的调查

禽白血病（avian leukosis,AL）是由禽白血病病毒（Avian Leukesis Virus,ALV）和禽肉瘤病毒（Avian Sarcoma Virus,ASV）群中的病毒引起的禽类多种肿瘤性疾病的统称,是近年来日益严重危害我国养禽业重要疫病之一。它可引起病鸡严重生长发育不良、受精率和孵化率等生产性能下降,同时可引发免疫抑制,导致机体抵抗力下降以及疫苗免疫效果不佳甚至失败并引起肿瘤死亡,因此该病一直是种鸡和蛋鸡生产中的重要疫病。近年来,我国陆续有报道ALV感染肉鸡群,但是在地方品种中的感染问题尚未完全弄清楚。     

蛋种鸡白血病净化研究

1净化意义禽白血病病毒(ALV)在自然条件下可通过饲料、饮水、孵化、输精、性别鉴定、污染粪便、疫苗及免疫接种等途径传播,带毒母鸡经蛋垂直传播给下一代。感染ALV的鸡其抗体产生动态规律是50日龄抗原阳性率开始上升,抗体阳性率低于10%。J亚群禽白血病病毒(ALV-J)抗原阳性率远大于A亚型禽白血病病毒(ALV-A)。ALV-J感染可显著干扰抗体产生,ALV-A感染则抗体水平较高。ALV感染鸡后会出现抗原阳性率上升而抗体阳性率下降的现象。     

Pathology of spontaneous tumour lesions in pullets and adult chickens in commercial farms - Short communication

Twenty pullets and adult chickens, aged 100 to 403 days, from several commercial chicken farms were examined by gross and histopathology. Grossly, all chickens had white-greyish masses in the visceral organs with or without enlargement of the peripheral nerves. Histopathological examination revealed Marek's disease (MD) lymphoma, lymphoid leukosis (LL) and myeloid leukosis (ML) in 14/20, 5/20 and 1/20 of the chickens, respectively. Lesions of the sciatic nerves in chickens diagnosed as having MD lymphoma were various. No neoplastic and/or inflammatory cells were noted in the peripheral nerves of chickens diagnosed as having LL and ML. These results indicated that MD lymphoma could also develop in older chickens; thus, microscopic examination is needed to identify MD in older chickens showing lymphocyte-derived tumours.     

Prevention of avian lymphoid leukosis by induction of bursal atrophy with infectious bursal disease viruses.

Five groups of genetically susceptible chickens were inoculated at hatching with lymphoid leukosis virus; four of these were given infectious bursal viruses of varying virulence at 14 days of age and one group was not inoculated (control). All chickens in the control group developed evidence of lymphoid leukosis by 180 days. Two groups given relatively virulent bursal disease viruses, which destroyed bursal lymphoid cells, did not develop lymphoid leukosis. Treatment with avirulent vaccines had no visible effect on bursal morphology and did not significantly alter the incidence of lymphoid leukosis in two other groups, although the time of development was delayed. Results of our study show that viral-induced destruction of the bursa of Fabricius eliminates the development of lymphoid leukosis but that infection without bursal destruction has little effect on lymphoid leukosis.     

Heterophil function and resistance to staphylococcal challenge in broiler chickens naturally infected with avian leukosis virus subgroup J

Avian leukosis virus subgroup J has a high tropism for myeloid lineage cells and frequently induces neoplastic transformation of myelocytes. The impact of congenital avian leukosis virus subgroup J infection on the function of circulating heterophils and susceptibility to staphylococcal infection was investigated. Six-week-old broiler chickens negative for exogenous avian leukosis viruses or congenitally infected with avian leukosis virus subgroup J were inoculated intravenously with 10(6) colony-forming units of Staphylococcus aureus, and pre- and postinoculation heterophil function was assessed. All chickens developed a leukocytosis with heterophilia after inoculation, but total leukocyte and heterophil counts were significantly higher in leukosis-negative chickens than in virus-infected chickens. Tenosynovitis was more severe in leukosis-negative chickens, and 2/10 (20%) of the virus-infected chickens had no histologic evidence of tenosynovitis. Osteomyelitis in the tibiotarsus or tarsometatarsus developed in 5/10 (50%) of the chickens in each group. S. aureus was recovered from the hock joint of 6/10 (60%) of the chickens in each group. Heterophils from all chickens exhibited similar phagocytic ability pre- and postinoculation. Heterophils from virus-infected chickens exhibited less bactericidal ability preinoculation than did heterophils from leukosis-negative chickens. However, postinoculation bactericidal ability was similar in both groups. Avian leukosis virus subgroup J provirus was present in heterophils isolated from congenitally infected chickens. Heterophils isolated from broiler chickens congenitally infected with avian leukosis virus subgroup J exhibit no significant functional deficits, and infected and uninfected chickens exhibit similar susceptibility to staphylococcal infection.     

Response of white leghorn chickens of various genetic lines to infection with avian leukosis virus subgroup J

In Experiment 1, chickens from various white leghorn experimental lines were inoculated with strain ADOL-Hcl of subgroup J avian leukosis virus (ALV-J) either as embryos or at 1 day of age. At various ages, chickens were tested for ALV-J induced viremia, antibody, and packed cell volume (PCV). Also, at 4 and 10 wk of age, bursal tissues were examined for avian leukosis virus (ALV)-induced preneoplastic lesions with the methyl green-pyronine (MGP) stain. In Experiment 2, chickens harboring or lacking endogenous virus 21 (EV21) were inoculated with strain ADOL-Hcl of ALV-J at hatch. All embryo-inoculated chickens in Experiment 1 tested positive for ALV-J and lacked antibody throughout the experimental period of 30 wk and were considered viremic tolerant, regardless of line of chickens. By 10 wk of age, the incidence of ALV-J viremia in chickens inoculated with virus at hatch varied from 0 (line 0 chickens) to 97% (line 1515); no influence of ALV-J infection was noted on PCV. Results from microscopic examination of MGP-stained bursal tissues indicate that ALV-J can induce typical ALV-induced transformation in bursal follicles of white leghorn chickens. Lymphoid leukosis and hemangiomas were the most common ALV-J-induced tumors noted in chickens in Experiment 1. At termination of Experiment 2 (31 wk of age), 54% of chickens harboring EV21 were viremic tolerant compared with 5% of chickens lacking EV21 after inoculation with ALV-J at hatch. The data indicate that genetic differences among lines of white leghorn chickens, including the presence or absence of EV21, can influence response of chickens to infection with ALV-J.     

用ALV-J gp85单克隆抗体证明蛋鸡存在J亚群禽白血病

采用免疫组化法，对病理学初步诊断为蛋用型鸡J亚群白血病的自然发病鸡的肿瘤、骨髓、肝脏、脾脏、肾脏、肺脏、心脏、胰脏、输卵管、卵巢、腺胃、骨骼肌、大脑、坐骨神经，用特异性抗J亚群禽白血病病毒(ALV—J)囊膜糖蛋白gp85的单克隆抗体进行检测，待检的组织切片中均检出阳性抗原，免疫组化的研究结果与病理学诊断结果相一致。在国内外首次发现并报道蛋用型鸡J亚群禽白血病的自然病例。     

Temporal changes of microRNA gga-let-7b and gga-let-7i expression in chickens challenged with subgroup J avian leukosis virus

Two important microRNAs, gga-let-7b and gga-let-7i were examined for the relative expression in liver and bone marrow tissues from specific pathogen free chickens that were challenged either with GD1109 or NX0101 strain of subgroup J avian leukosis virus (ALV-J). The GD1109 strain of ALV-J reportedly causes hemangioma (HE) and NX0101 reportedly causes myeloma (ML) in susceptible chickens. Temporal changes of both gga-let-7b and gga-let-7i expression in ALV-J infected chickens were observed in contrast to its counterpart of a non-infected negative control group of chickens (P < 0.05 or P < 0.01) during the first 120 days post infection. Use of the web-based computational DIANA-mirPath software (available at http://microrna.gr/mirpath), it was predicted that both gga-let-7b and gga-let-7i were involved in multiple pathways including signaling pathways, such as MAPK, TGF-beta, Notch, Wnt, mTOR, Cell cycle, P53 and Jak-STAT. Combining our experimental data with reports on the microRNAs, we suggest that both gga-let-7i and gga-let-7b may also act as tumor suppressors in chicken, especially play a critical role in tumorigenesis induced by ALV-J.     

Field trials to test the efficacy of polyvalent Marek's disease vaccines in broilers

The efficacies of trivalent (Md11/75C + SB-1 + HVT), bivalent (SB-1 + HVT), and turkey herpesvirus (HVT) vaccines against Marek's disease (MD) were compared in commercial broiler flocks in four trials involving 11 farm locations and 486,300 chickens. In all four trials, chickens receiving polyvalent vaccines had lower leukosis (MD) condemnation rates than chickens vaccinated with HVT alone; when data were summarized for each vaccine type in each trial, condemnation rates for the bivalent- or trivalent-vaccinated groups were 56-96% (mean 78%) lower than those for HVT-vaccinated chickens. Polyvalent vaccination was clearly mor efficacious than HVT in 8 of 11 individual farms, although it did not always reduce leukosis condemnations to acceptable levels. Body weights of chickens vaccinated with polyvalent vaccines did not differ consistently from those vaccinated with HVT. Chickens inoculated with the trivalent vaccine had slightly lower overall leukosis condemnation rates (0.24%) than those inoculated with the bivalent vaccine (0.45%) in trials 1-3, where direct comparisons were made. Bivalent vaccines containing either 1,500 or 200 plaque-forming units of SB-1 virus were equally effective; thus, HVT may need to be supplemented with only small amounts of SB-1 to obtain the benefits of protective synergism. SB-1 virus did not appear to carry over from polyvalent-vaccinated flocks to subsequent HVT-vaccinated flocks in the same houses, even when old litter was used.     

Molecular and biological characterization of a naturally occurring recombinant subgroup B avian leukosis virus with a subgroup J-like long terminal repeat

Infection of broiler chickens with subgroup J avian leukosis virus (ALV) results in the induction of myeloid tumors. However, although egg-type chickens are susceptible to infection with ALV-J, the tumor incidence is very low, and on rare occasions the tumors observed are of the myeloid lineage. We recently described the isolation of an ALV (AF115-4) from commercial egg-type chickens suffering from myeloid leukosis. AF115-4 was initially identified as an ALV-J isolate based on PCR analysis of the long terminal repeat (LTR). However, further characterization of the viral envelope indicated that the virus is recombinant with subgroups B envelope and J LTR. Here we further characterize this recombinant virus at both the molecular and biological levels. We show that the AF115-4 isolate expresses a recombinant envelope glycoprotein encoded by a subgroup B gp85 region and a subgroup E gp37 region. The host range ofAF115-4 was analyzed using cells resistant to infection by subgroups A/B, J, or E; this shows that no ALV-J was present in the isolates obtained from the affected chickens. Additional antigenic characterization of AF115-4 using chicken sera specific for subgroups B or J indicated that no ALV-J was present in the samples examined. Inoculation of AF 115-4 into ALV-susceptible 1515 X 71 chickens resulted in the induction of lymphoid leukosis but not the expected myeloid leukosis affecting the commercial chickens. These results suggest that differences in the genetic makeup of the chickens from which AF115-4 was isolated and the line 1515 X 71 used in the present experiments may be responsible for the observed differences in pathogenicity. In addition, the results suggest that ALV-J continues to evolve by recombination, generating new viruses with different pathological properties.     

Sarcomas and myelocytomas induced by a retrovirus related to myeloblastosis-associated virus type 1 in White Leghorn egg layer chickens

An outbreak of subcutaneous sarcomas in commercial White Leghorn egg layers was observed in the northeastern United States during late 2004. Subcutaneous tumors were confined to three flocks distributed in two locations and belonging to the same company. The tumors were first observed grossly by farm personnel at approximately 7 wk of age and persisted throughout the economic life of the flocks. Most of the tumors observed during the growing period were present on the facial region or around the head, wings, and legs. There was no gross evidence of bursal or visceral involvement. Microscopically, most tumors were undifferentiated sarcomas and myxomas. There was no microscopic evidence of Marek's disease or lymphoid leukosis. Reticuloendotheliosis virus proviral DNA was not detected by polymerase chain reaction either in tumors or in cell cultures. Egg production and mortality rates were within normal limits in the affected flocks and many of the chickens exhibiting tumors seemed healthy otherwise, albeit approximately one-half of the daily mortality exhibited tumors. Avian myeloblastosis-associated virus type 1 (MAV-1) was isolated from tumors, plasma, and serum. Upon initial virus neutralization, the viruses isolated seemed at least partially related antigenically to avian leukosis virus (ALV) subgroups A and B but not to subgroup J (ALV-J). Sequencing of the variable and hypervariable regions of gp85 in the envelope gene revealed that the viruses involved are closely related to MAV-1. Attempts to reproduce subcutaneous sarcomas with MAV-1 isolated from White Leghorn chickens in the case herein reported produced exclusively myelocytomas indistinguishable histologically from those induced by ALV-J in meat type chickens.     

The effects of avian leukosis virus subgroup J on broiler chicken performance and response to vaccination

The effects of avian leukosis virus subgroup J (ALV-J) infection on meat-type chickens reared in a simulated commercial setting were evaluated. Each of three ALV-J isolates was evaluated with both simulated horizontal transmission (SHT) and simulated vertical transmission (SVT). Mortality, morbidity, disease condemnations, and feed conversions were increased and body weights at processing were decreased in ALV-J infected birds as compared to sham inoculated hatch mates. The adverse effects of ALV-J infection were more severe in birds exposed by SVT than in birds exposed by SHT. At 8 weeks of age response to vaccination for infectious bronchitis virus and Newcastle disease virus or prior exposure to a pathogenic reovirus was assessed in the ALV-J and sham inoculated broiler chickens by challenge studies. Although not statistically significant, an overall trend of decreased protection to challenge after vaccination, or prior exposure, was observed in the ALV-J inoculates as compared to sham inoculated hatch mates. Differences in vaccine response were most evident in groups inoculated with ALV-J by the SVT route.