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1.
Cui Z  Sun S  Wang J 《Avian diseases》2006,50(2):191-195
In this study, a Chinese field strain of subgroup J avian leukosis virus (ALV-J), NX0101, was studied for its immunosuppressive effects in both commercial broilers and SPF white Leghorn chickens infected at 1 day of age. Our data demonstrated that NX0101 induced much more significant body and immune organ weight loss in the infected commercial broiler chickens in an earlier age than that in the SPF white Leghorn chickens. At the same time antibody responses to vaccinations of Newcastle disease virus (NDV) and infectious bursa disease virus (IBDV) in the NX0101-infected chickens were also evaluated and compared between the commercial broiler chickens and the SPF white Leghorn chickens. Compared with the control group of chickens, the hemagglutination inhibition (HI) antibody response to NDV vaccines was significantly reduced in the NX0101-infected commercial broiler chickens from as early as 20 days after vaccination. However, no significant difference in HI antibody response was seen when HI titers reached their peaks in the NX0101-inoculated and control SPF white Leghorn chickens, except it declined significantly faster in infected birds. Neither of these two types of chickens showed significant decrease of antibody response to IBDV vaccination. Herein, we conclude that this NX0101 strain of ALV-J could selectively suppress humoral immune reactions to NDV, especially in broilers. But challenge experiments were not conducted and, therefore, it cannot be known if decreased antibody levels correlated with decreased protection against NDV in this case.  相似文献   

2.
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.  相似文献   

3.
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.  相似文献   

4.
Lai H  Zhang H  Ning Z  Chen R  Zhang W  Qing A  Xin C  Yu K  Cao W  Liao M 《Veterinary microbiology》2011,151(3-4):275-283
Subgroup J avian leukosis virus (ALV-J), first isolated in 1989, predominantly causes myeloid leukosis (ML) in meat-type or egg-type chicken. Since 2006, the clinical cases of hemangioma rather than ML in commercial layer flocks associated with ALV-J have been reported, but it was still not clear whether the novel oncogenic ALV-J had emerged. We characterized SCAU-HN06 isolate of ALV-J from hemangioma in commercial Roman layers through animal experiment and full-length proviral genome sequence analysis. The SPF white leghorn egg-type chickens infected with SCAU-HN06 in ovo at day 11 of incubation showed an overall incidence of 56% hemangioma and 8% renal tumor throughout the 22-week trial, the mortality rate was 16%. Most genes of SCAU-HN06 isolate showed high nucleotide sequence identity to JS09GY6 which was isolated from Hy-Line Variety Brown layers suffering hemangioma. The 19-bp insertion in leader sequence and one key deletion in E element were the common features of SCAU-HN06 and JS09GY6. SCAU-HN06 and those ALV-Js associated with hemangioma, possibly recombinants of ALV-J and other avian retrovirus, may share the same ancestor.  相似文献   

5.
6.
Zavala G  Cheng S 《Avian diseases》2006,50(2):232-237
Recently, avian leukosis virus (ALV) was isolated from four lots of Marek's disease vaccine produced by two laboratories. The ALVs isolated were characterized by examination of their interactions with cells of two phenotypes (C/E and C/A,E), subgroup-specific polymerase chain reaction (PCR), virus neutralization, envelope gene sequencing, and phylogenetic analysis. All four ALVs are exogenous, belong to subgroup A, and appear to be virtually identical to each other based on PCR and envelope gene nucleotide sequences. We describe herein the characterization of the contaminant viruses in vivo by means of experimental infection in chickens. The contaminant viruses established transient viremia in specified pathogen-free (SPF) Leghorn chickens and elicited a robust and lasting antibody response detectable by enzyme-linked immunosorbent assay. None of the contaminant ALVs induced tumors up to 31 wk of age, and mortality was insignificant. Despite a strong antibody response against the contaminant ALVs, vertical (congenital) transmission to the progeny of experimentally infected SPF chickens took place, albeit at a very low rate (< or = 1.6%). Experimental infection in meat-type chicken embryos resulted in viremia at hatch, suggesting that some meat-type chickens are susceptible to infection and support virus replication.  相似文献   

7.
Lu H  Castro AE 《Avian diseases》2004,48(2):263-270
The H7N2 subtype of avian influenza virus (AIV) field isolate (H7N2/chicken/PA/3779-2/97), which caused the 1997-98 AIV outbreak in Pennsylvania, was evaluated for its infectivity, length of infection, and immune response in specific-pathogen-free (SPF) chickens. The composite findings of three clinical trials with various concentrations of virus indicated that this H7N2 subtype contained minimal pathogenicity for chickens. The concentration of the virus in the inoculum proved critical in the establishment of a productive infection in a chicken. Seven-day-old SPF chickens were not infected when inoculated with 10(0.7-2.0) mean embryo lethal dose (ELD50) of the H7N2 virus per bird. At this dose level, the immune response to this virus was not detected by the hemagglutination-inhibition (HI) test. Nonetheless, chickens at ages of 5 and 23 wk old tested were successfully infected when exposed to 10(4.7-5.7) ELD50 of H7N2 infectious doses per bird by various routes of administration and also by direct contact. Infected birds started shedding virus as early as 2 days postinoculation, and the period of virus shedding occurred mostly within 1 or 2 wk postinoculation (WPI). This H7N2 subtype of AIV induced a measurable immune response in all birds within 2 wk after virus exposure. Antibody titers were associated with AIV infectious doses and age of exposure of birds. Challenge of these infected birds with the same H7N2 virus at 5 and 10 WPI indicated the infective virus was recoverable from cloacal swabs at 3 days postchallenge and disappeared thereafter. In these challenged birds, the antibody levels as measured by the HI test spiked within 1-2 wk.  相似文献   

8.
White leghorn chickens from seven 15.B congenic lines (genetically similar except for genes linked to the major histocompatibility complex [MHC] B haplotype) and two Line 0.B semicongenic lines were infected at hatch with strain ADOL Hc-1 of subgroup J avian leukosis virus (ALV-J). At 5, 8, 16, and 36 wk of age, chickens were tested for viremia, serum-neutralizing antibody, and cloacal shedding. Chickens were also monitored for development of neoplasia. In the 15.B congenic lines (B*2, B*5, B*12, B*13, B*15, B*19, and B*21) there were no significant differences in the incidence of viremia between B haplotypes. In fact, infection at hatch in all of the 15.B congenic lines induced tolerance to ALV-J because 100% of these chickens were viremic and transient circulating serum-neutralizing antibody was detected in only a few chickens throughout the 36 wk experiment. However, at 16 wk of age more B*15 chickens had antibody and fewer B*15 chickens shed virus than did the 16-wk-old B*2, B*5, or B*13 chickens. Moreover, compared with B*15 chickens, a higher percentage of B*13 chickens consistently shed virus from 8 wk postinfection to termination at 36 wk postinfection. The B haplotype had a transient effect on viral clearance in Line 0.B semicongenics, as more B*13 than B*21 chickens remained viremic through 5 wk of age. Very few (0%-18%) of the Line 0.B semicongenic chickens shed virus. By 36 wk of age, all Line 0 B*13 and B*21 chickens produced serum-neutralizing antibodies and cleared the virus. These results show that following ALV-J infection at hatch the immune response is influenced transiently by the B haplotype and strongly by the line of chicken. Although this study was not designed to study the effect of endogenous virus on ALV-J infection, the data suggest that endogenous virus expression reduced immunity to ALV-J in Line 15I5, compared with Line 0, a line known to lack endogenous virus genes.  相似文献   

9.
本研究采用AGP、HI等试验方法,对经H9亚型禽流感油乳剂灭活苗免疫、免疫后攻毒以及经H9N2活毒人工感染后的SPF鸡抗体产生、消长规律进行了测定,结果表明人工感染SPF鸡和免疫鸡一周后,AGP的检出率即可达到100%;H9亚型禽流感油乳剂灭活苗自免疫后一周内即可产生HI抗体,21-28天达到高峰,并能对相同亚型病毒感染引发良好的免疫反应。  相似文献   

10.
To monitor the existence of avian pathogens in laying chicken flocks, specific pathogen-free (SPF) chickens were introduced into two layer farms and reared with laying hens for 12 months. SPF chickens were bled several times after their introduction and examined for their sero-conversion to avian pathogens. As a result, antibodies to eight or ten kinds of pathogens were detected in SPF chickens on each farm. Antibodies to infectious bronchitis virus (IBV), avian nephritis virus, Mycoplasma gallisepticum and M. synoviae were detected early within the first month. Antibody titer to IBV suggested that the laying chickens were infected with IBV repeatedly during the experiment on both farms. However, antibodies to infectious bursal disease virus and 6 pathogens were not detected.  相似文献   

11.
Ten-day-old chickens infected with an avian osteopetrosis virus [MAV-2(O)] were more susceptible to challenge with Listeria monocytogenes than virus-free chickens, as demonstrated by reduced bacterial clearance from their spleens. Reduced clearance of L. monocytogenes was observed throughout a 26-day period after MAV-2(O) infection.  相似文献   

12.
Sung HW  Reddy SM  Fadly AM 《Avian diseases》2002,46(2):281-286
Subgroup J avian leukosis viruses (ALVs), which are a recombinant virus between exogenous and endogenous ALVs, can spread by either vertical or horizontal transmission. Exogenous and endogenous ALVs can be detected in feather pulp. In this study, virus titers in feather pulp of chickens infected with subgroup J ALV were compared with those of plasma and cloacal swab. All of the broiler chickens inoculated with subgroup J ALV at 1 day old were positive for virus from feather pulp during the experimental period of between 2 wk and 8 wk of age. Virus titers in feather pulp of some broiler chickens infected with subgroup J ALV were very high, ranging from 10(7) to 10(8) infective units per 0.2 ml. Virus titers in feather pulp were usually the highest among the samples of plasma, cloacal swab, and feather pulp tested. In another experiment in which layer chickens were inoculated with subgroup J ALV at 1 day old, virus was detected in feather pulp from 2 wk until 18 wk of age, and virus persisted longer in feather pulp than in plasma. Almost all of the layer chickens tested were positive for virus by polymerase chain reaction (PCR) with DNA extracted from feather pulp samples at 2, 4, and 10 wk of age, and the PCR from feather pulp was more sensitive than virus isolation from plasma, cloacal swab, and feather pulp. All above results indicate that samples of feather pulp can be useful for virus isolation and PCR to confirm subgroup J ALV infection.  相似文献   

13.
The pathogenicity and transmission of a field isolate of reticuloendotheliosis virus (REV) was studied using an experimental model in Japanese quail. Oncogenicity was also evaluated after inoculations in chickens and turkeys. The original REV (designated APC-566) was isolated from Attwater's prairie chickens (Tympanuchus cupido attwateri), an endangered wild avian species of the southern United States. The transmissibility of the REV isolate was studied in young naive Japanese quail in contact with experimentally infected quail. Vertical transmission was not detected by virus isolation and indirect immunofluorescence. Seroconversion was detected in few contact quails, suggesting horizontal transmission. The APC-566 isolate induced tumors beginning at 6 wk of age in quails infected as embryos. Most of the tumors detected in Japanese quail were lymphosarcomas, and 81% of these neoplasias contained CD3+ cells by immunoperoxidase. REV APC-566 was also oncogenic in chickens and turkeys infected at 1 day of age, with tumors appearing as early as 58 days after infection in chickens and at 13 wk of age in turkeys. This study was conducted in part as an attempt to understand the potential for pathogenicity and transmission of REV isolated from endangered avian species.  相似文献   

14.
用ALV-J gp85单克隆抗体证明蛋鸡存在J亚群禽白血病   总被引:20,自引:1,他引:20  
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。  相似文献   

15.
The California poultry industry experienced an outbreak of H6N2 avian influenza beginning in February 2000. The initial infections were detected in three commercial egg-laying flocks and a single noncommercial backyard flock but later spread to new premises. The vaccination of pullet flocks with a commercially prepared, killed autogenous vaccine prior to their placements on farms with infected or previously infected flocks was used as a part of the eradication programs for some multiage, commercial egg production farms. The purpose of this study was to follow three vaccinated flocks on two commercial farms to track the immune responses to vaccination. The antibody-mediated responses of the three flocks followed in this study were markedly different. One flock achieved 100% seroconversion at 12.5 wk of age, but by 32 wk of age, all of the hens were seronegative by agar gel immunodiffusion (AGID). In contrast, at 32 wk of age, flocks from the other farm (flocks 2A and 2B) were 95% and 72% seropositive by AGID, respectively. Of the differences that were identified between the vaccination protocols on the two farms, the distinction that could explain the level of disparity between responses is the delivery of the second dose of vaccine with a bacterin on the first farm, which may have interfered with the persistence of immunity in this flock. Hens from flocks 2A and 2B were experimentally challenged at 25 wk of age with H6N2 avian influenza virus. Hens from flock 2A did not transmit virus to naive contact-exposed hens, but hens from flock 2B did. At 34 wk of age, hens from flock 2A were again challenged and naive contact-exposed hens were infected in this second trial. These challenge experiments served to demonstrate that despite detectable antibody responses in flocks 2A and 2B, the birds were protected from infection for less than 21 wk after the second vaccination.  相似文献   

16.
Experimental infection of specific-pathogen-free (SPF) Leghorn chickens with a highly pathogenic H5N2 avian influenza virus produced cellular hyperplasia in the bone marrow at 36 hours post infection (hpi) and haematological evidence of monocytosis, thrombocytopenia and heterophilia was also detected. An early, significant and progressive haematological change was thrombocytopenia starting at 24 hpi without an increase of prothrombin time. The findings suggest that highly pathogenic avian influenza virus interferes only with the primary haemostatic mechanisms by consumption of thrombocytes, while the secondary haemostatic mechanisms remain intact.  相似文献   

17.
CAV与REV共感染SPF鸡对疫苗免疫反应的抑制作用   总被引:3,自引:0,他引:3  
用1日龄SPF鸡人工感染鸡贫血病毒(CAV)和禽网状内皮增生病病毒(REV),探讨病毒感染对鸡体疫苗免疫反应的影响。结果表明,在用禽流感病毒(AIV,H5和H9)疫苗免疫后,CAV与REV单独感染均显著抑制了鸡体对H5和H9亚型禽流感病毒灭活疫苗的HI抗体反应,在CAV与REV共感染后,这种抑制作用更为明显。CAV单独感染后鸡体对新城疫病毒(NDV)和传染性法氏囊病病毒(IBDV)疫苗的免疫反应受到抑制,但与对照组在统计学上的差异不显著,然而,CAV可以显著加重REV感染对鸡体在NDV和IBDV疫苗免疫后抗体反应的抑制作用。从而证实CAV与REV共感染在疫苗免疫抑制上有协同作用。  相似文献   

18.
鸡传染性支气管炎病毒(IBV)具有不同致病特性,将IBV XDC-2株接种9日龄SPF鸡胚培养,可引起鸡胚死亡和出现侏儒胚,病毒EID50达5×10-5.33/mL。将IBV XDC-2株接种18日龄SPF鸡,饲养观察14 d,病鸡临床症状表现为:精神沉郁,羽毛凌乱,双翅下垂,轻微腹泻,多数拉白色水样稀粪。病死鸡出现肾肿大、呈花斑状、大量尿酸盐沉积。鸡发病率为100%,死亡率为25%。死亡鸡肺脏、肾组织制作组织切片,发现病理变化明显,主要为:肾小管扩张,上皮细胞呈玻璃样变性,部分管腔内可见坏死脱落之上皮细胞,于肾间质可见大量单核细胞浸润,肾间质有充血、出血现象;肺内动脉、毛细血管充血,淋巴细胞浸润。死亡鸡肺脏、肾组织接种鸡胚分离病毒,RT-PCR检测结果为阳性,表明该分离株为鸡传染性支气管炎病毒,具有很强的嗜肾性。  相似文献   

19.
ALV-J和REV诱导雏鸡胸腺细胞凋亡   总被引:2,自引:1,他引:1  
应用原位末端标记法和HE染色法对人工感染J亚群禽白血病病毒(ALV-J)和禽网状内皮增生症病毒(REV)的SPF雏鸡胸腺细胞的凋亡情况进行了检测,同时辅以电镜超薄切片观察。结果表明,ALV-J和REV均可诱导雏鸡胸腺细胞发生凋亡,混合感染诱导的细胞凋亡更加严重;切片中可出现局灶状凋亡,凋亡细胞多于坏死细胞。研究结果表明,细胞凋亡是导致感染鸡胸腺萎缩的主要原因。  相似文献   

20.
为了检测从国外直接进口的蛋用型祖代鸡群是否存在外源性禽白血病病毒(ALV)的感染,将240只1日龄鸡饲养在严格的SPF环境中。在不同日龄采集泄殖腔棉拭子检测ALV群特异性p27抗原、采集血浆分离外源性ALV和采集血清检测ALV-AB及J特异性抗体。结果表明:在近3个月的6次采样检测中,6个不同的配套系间泄殖腔棉拭子检出率显著不同。其中1个配套系6次完全阴性,其余5个则在不同时期呈间隙性阳性。各品系之间ALV p27抗原检出率与快慢羽性状没有相关性。慢羽的配套系C,36只鸡中在45日龄检出了1例ALV-AB抗体一过性阳性,在60日龄检出了2例ALV-J抗体一过性阳性。分别在5、21日龄采血浆在DF1细胞分离病毒,所有的6个配套系的204只鸡外源性ALV的病毒分离均为阴性。  相似文献   

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