Susceptibility of various parental lines of commercial white leghorn layers to infection with a naturally occurring recombinant avian leukosis virus containing subgroup B envelope and subgroup J long terminal repeat

Chickens from seven different parental lines of commercial White Leghorn layer flocks from three independent breeders were inoculated with a naturally occurring avian leukosis virus (ALV) containing an ALV-B envelope and an ALV-J long terminal repeat (LTR) termed ALV-B/J. Additional groups of chickens from the same seven parental lines were inoculated with ALV-B. Chickens were tested for ALV viremia and antibody at 0, 4, 8, 16, and 32 wk postinfection. Chickens from all parental lines studied were susceptible to infection with ALV-B with 40%-100% of inoculated chickens positive for ALV at hatch following embryo infection. Similarly, infection of egg layer flocks with the ALV-B/J recombinant virus at 8 days of embryonation induced tolerance to ALV with 86%-100% of the chickens viremic, 40%-75% of the chickens shedding virus, and only 2/125 (2%) of the chickens producing serum-neutralizing antibodies against homologous ALV-B/J recombinant virus at 32 wk postinfection. In contrast, when infected with the ALV-B/J recombinant virus at hatch, 33%-82% of the chickens were viremic, 28%-47% shed virus, and 0%-56% produced serum-neutralizing antibodies against homologous ALV-B/J recombinant virus at 32 wk postinfection. Infection with the ALV-B/J recombinant virus at embryonation and at hatch induced predominately lymphoid leukosis (LL), along with other common ALV neoplasms, including erythroblastosis, osteopetrosis, nephroblastomas, and rhabdosarcomas. No incidence of myeloid leukosis (ML) was observed in any of the commercial White Leghorn egg layer flocks infected with ALV-B/J in the present study. Data suggest that the parental line of commercial layers may influence development of ALV-B/J-induced viremia and antibody, but not tumor type. Differences in type of tumors noted in the present study and those noted in the field case where the ALV-B/J was first isolated may be attributed to differences in the genetics of the commercial layer flock in which ML was first diagnosed and the present commercial layer flocks tested in the present study.     

Isolation and some characteristics of a subgroup J-like avian leukosis virus associated with myeloid leukosis in meat-type chickens in the United States.

Several subgroup J-like avian leukosis viruses (ALV-Js) were isolated from broiler breeder (BB) and commercial broiler flocks experiencing myeloid leukosis (ML) at 4 wk of age or older. In all cases, diagnosis of ML was based on the presence of typical gross and microscopic lesions in affected tissues. The isolates were classified as ALV-J by 1) their ability to propagate in chicken embryo fibroblasts (CEF) that are resistant to avian leukosis virus (ALV) subgroups A and E (C/AE) and 2) positive reaction in a polymerase chain reaction with primers specific for ALV-J. The prototype strain of these isolates, an isolate termed ADOL-Hc1, was obtained from an adult BB flock that had a history of ML. The ADOL-Hc1 was isolated and propagated on C/AE CEF and was distinct antigenically from ALV of subgroups A, B, C, D, and E, as determined by virus neutralization tests. Antibody to ADOL-Hc1 neutralized strain HPRS-103, the prototype of ALV-J isolated from meat-type chickens in the United Kingdom, but antibody to HPRS-103 did not neutralize strain ADOL-Hc1. On the basis of both viremia and antibody, prevalence of ALV-J infection in affected flocks was as high as 87%. Viremia in day-old chicks of three different hatches from a BB flock naturally infected with ALV-J varied from 4% to 25%; in two of the three hatches, 100% of chicks that tested negative for virus at hatch had evidence of viremia by 8 wk of age. The data document the isolation of ALV-J from meat-type chickens experiencing ML as young as 4 wk of age. The data also suggest that strain ADOL-Hc1 is antigenically related, but not identical, to strain HPRS-103 and that contact transmission of ALV-J is efficient and can lead to tolerant infection.     

Tissue tropism and bursal transformation ability of subgroup J avian leukosis virus in White Leghorn chickens

In Experiment 1, a monoclonal antibody against the envelope glycoprotein (gp85) of subgroup J avian leukosis virus (ALV-J) was used to study the distribution of ALV-J in various tissues of White Leghorn chickens inoculated as embryos with the strain ADOL-Hcl of ALV-J. At 2 and 6 wk of age, various tissues from infected and control uninfected chickens were tested for the presence of ALV-J gp85 by immunohistochemistry. In Experiment 2, using the methyl green-pyronine (MGP) stain, sections of bursa of Fabricius (BF) from chickens of line 15I5 x 7(1), inoculated with ALV-J or Rous-associated virus-1 (RAV-1), a subgroup A ALV, at hatch were examined for transformation of bursal follicles at 4 and 10 wk of age. In Experiment 1, specific staining indicative of the presence of ALV-J gp85 was noted at both 2 and 6 wk of age in the adrenal gland, bursa, gonads, heart, kidney, liver, bone marrow, nerve, pancreas, proventriculus, spleen, and thymus. In Experiment 2, by 10 wk of age, transformed bursal follicles were detected in MGP-stained sections of BF in only one of five (20%) chickens inoculated with ALV-J at hatch, compared with five of five (100%) chickens inoculated with RAV-1. The data demonstrate distribution of ALV-J gp85 in various tissues of White Leghorn chickens experimentally inoculated as embryos with the virus. The data also confirm our previous observation that ALV-J is capable of inducing transformation of bursal follicles, albeit the incidence is less frequent than that induced by subgroup A ALV.     

Natural infection and transmission of a retrovirus closely related to myeloblastosis-associated virus type 1 in egg-type chickens

Myeloblastosis-associated virus type 1 (MAV-1) is an exogenous avian retrovirus with oncogenic potential. MAV-1 was detected in young chicks hatching from eggs produced by an experimental genetic line of egg-type chickens. Transmissibility of MAV-1 had not been documented previously. This investigation was intended to partially characterize the virus involved and to study its transmissibility and oncogenicity in naturally and contact-infected chickens. Commercially produced white and brown layer pullets free of exogenous avian leukosis viruses were commingled at hatch with naturally MAV-1-infected chickens. The original MAV-1-infected chickens were discarded after approximately 8 wk, and the contact-exposed chickens were maintained in isolation for 36 wk. Young specific-pathogen-free (SPF) single comb white leghorn chickens were added to the group to study possible horizontal transmission of MAV-1 in young chickens. Upon weekly virus isolation attempts, MAV-1 was readily isolated from the contact-exposed white layers but not from the brown layers between 36 and 53 wk of age (18 wk in total). Three-week-old SPF chickens were readily infected with MAV-1 by contact as early as 1 wk postexposure. Throughout 22 hatches derived from the white and brown MAV-1-contact-exposed layers (between 36 and 53 wk of age), MAV-1 was frequently detected in the white layer progeny, whereas the virus was seldom isolated from the progeny produced by the brown layers during the same 18-wk period. MAV-1 induced a persistent infection in some of the SPF chickens that were exposed by contact at 3 wk of age. Gross tumors were not detected in any of the originally infected experimental chickens at 8 wk of age, in the contact-exposed brown or white layers at the termination of the study at 53 wks of age, or in the contact-exposed SPF chickens at the end of the study at 12 wk of age. Exogenous avian leukosis-related viruses may still be detected in egg-type chickens, emphasizing the importance of thorough screening before incorporation of experimental genetic material into commercial genetic lines of egg-type chickens.     

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.     

On epizootiology and control of lymphoid leukosis in chickens

Sera and organ extracts from ten different commercial stocks of layer chickens were examined for the presence of lymphoid leukosis (LL) viruses. Virus was recovered from 40.8% of the cockerels between three and six weeks of age. Their female hatch mates were examined at the age of 20 months. A mean of 11.3% of these laying hens was positive in the NP activation test. Lymphoid leukosis was successfully controlled in three inbred strains of White Leghorn chickens and in a commercial White Plymouth Rock line. All flocks were kept in a filtered air positive pressure (FAPP) house during the first two months of life and thereafter transferred to a conventional environment. The control method is based on three elements:

• —from an infected flock, hens are selected in whose eggs no avian lymphoid leukosis viruses can be detected by examination of pooled extracts of groups of embryos;

• —only eggs from hens that are shown not to shed congenitally virus in their eggs are used for the production of progeny. The offspring are reared in isolation until two months of age at which time the age-related resistance against tumour formation appears to be sufficiently developed;

• —the chickens are subsequently intramuscularly inoculated with lymphoid leukosis viruses of subgroups A and B and transferred to a conventional chicken house. The inoculated birds become persistently viremic and resist horizontal virus exposure and intramuscular challenge infections.

Horizontal virus transmission was observed to take place when virus-free non-vaccinated chickens were reared in isolation for two months and then exposed under field conditions.Efficiency of virus recovery was considerably improved when washed buffy coat cells were cocultivated with chick embryo fibroblasts or explant cultures were prepared from various tissues before testing with the NP activation test.     

某海兰褐鸡场祖代、父母代及商品代鸡血管瘤型ALV-J的分离与鉴定

从山东省某海兰褐鸡场祖代、父母代种鸡和商品代蛋鸡中获得疑似血管瘤型禽白血病(Avian leukosis,AL)病料.采用病理剖检、IFA、分子生物学检测,确定为J亚群禽白血病.从祖代、父母代病料中各分离到1株J亚群禽白血病病毒(J subgroup of avian leukosis virus,ALV-J),从商品代蛋鸡中分离到4株ALV-J.根据原型毒株HPRS103设计1对gp85基因引物,获得gp85基因序列.获得的gp85基因序列与各亚群参考毒株序列核苷酸同源性比对,结果显示:分离自商品代蛋鸡的Commercial03株、Commercial04株、Commercial06株和父母代分离株Parent02株位于同一分支,同源性在97.2％～97.9％,与HPRS103株同源性94.7％～95.2％;Commercial05株与祖代分离株Grandparent01株在同一分支,与HPRS103株同源性为98.3％,4株分离自商品代的ALV-J同源性为95.0％～99.9％.表明商品代蛋鸡中的ALV-J可能来自父母代或祖代种鸡的垂直传播,也可能来自于其他来源的水平传播.从同一鸡场祖代、父母代及商品代鸡中分离得到ALV-J,这在我国还是首次.对后续研究其基因突变、致瘤机制等奠定了良好的基础.     

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.     

Detection of subgroup J avian leukosis virus infection in Australian meat-type chickens

OBJECTIVE: To determine the extent of avian leukosis virus subgroup J (ALV-J) infection in Australian broiler breeder flocks, using virus isolation and molecular biological detection. Any resultant ALV-J viral isolates to be characterised by neutralisation cross testing in order to determine antigenic relationships to overseas isolates of ALV-J. STUDY DESIGN: Samples of blood, feather pulp, albumen and tumours were obtained from broiler breeder flocks which represented four genetic strains of meat chickens being grown in Victoria, South Australia, NSW and Queensland. Dead and ailing birds were necropsied on farm and samples were collected for microscopic and virological examinations. Virus isolation was carried out in C/O and DF-1 CEF cultures and ALV group specific antigen was detected in culture lysates using AC-ELISA. Micro-neutralisation assay was used for antigenic characterisation of selected isolates. Genomic DNA was isolated from cultured cells, tumours and feather pulp. ALV-J envelope sequences were amplified by PCR using specific ALV-J primers while antibodies against ALV-J were detected by ELISA. RESULTS: A total of 62 ALV-J isolates were recovered and confirmed by PCR from 15 (31.3%) of 48 breeder flocks tested. Antibody to ALV-J was detected in 20 (47.6%) of the 42 flocks tested. Characteristic lesions of myeloid leukosis caused by ALV-J were found in affected flocks. The gross pathological lesions were characterised by skeletal myelocytomas located on the inner sternum and ribs, neoplastic enlargement of the liver, and in some cases gross tumour involvement of the spleen, kidney, trachea, skeletal muscles, bone marrow, skin and gonads. Microscopically, the tumours consisted of immature granulated myelocytes, and were present as focal or diffuse infiltrations in the affected organs. Virus micro-neutralisation assays demonstrated antigenic variation among Australian isolates and to overseas strains of ALV-J. CONCLUSION: ALV-J infection was prevalent in Australian broiler breeder flocks during 2001 to 2003. Australian isolates of ALV-J show a degree of antigenic variation when compared to overseas isolates.     

Reduced serologic response to Newcastle disease virus in broiler chickens exposed to a Chinese field strain of subgroup J avian leukosis virus

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.     

Isolation and characterization of emerging subgroup J avian leukosis virus associated with hemangioma in egg-type chickens

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.     

表现腺胃炎的蛋用型鸡J亚群-白血病病毒的分离与鉴定

从表现腺胃炎的尼克珊瑚粉商品代蛋鸡中分离到J亚群-白血病病毒(ALV-J)。将病料或鸡白细胞接种于CEF,培养12 d,分别采用单克隆抗体间接免疫荧光试验检测,结果10只鸡中有9只鸡分离到ALV-J,其中有4只鸡还存在与禽网状内皮增生病病毒(REV)的共感染。通过PCR扩增gp85基因,与已发表的20株ALV-J进行同源性比较。结果表明,与来自白羽肉鸡的HPRS103的同源性为97.8%,而与来自蛋用型鸡的SD07LK1株的同源性为93.0%。本研究发现,在某些仅仅发生腺胃炎的鸡也可能普遍存在ALV-J感染,再次显示了腺胃炎病料中病毒感染的多样性。ALV-J可能成为致腺胃炎的病原之一,但其致病作用有待进一步研究。     

Genetic diversity and phylogenetic analysis of glycoprotein GP85 of ALV-J isolates from Mainland China between 1999 and 2010: coexistence of two extremely different subgroups in layers

Avian leukosis virus subgroup J (ALV-J), first isolated in 1989, preferentially infects meat-type birds. However, layer flocks in China have experienced outbreaks of this virus since 2008. To understand the genetic diversity of ALV-J in Chinese layers, we compared and analyzed the GP85 gene sequences of 106 ALV-J isolates that were isolated between 1999 and 2010 in Mainland China. The GP85 gene sequences of 41 layer isolates collected from 9 provinces of China between 2008 and 2010 belonged to two separate, highly diverse subgroups and were differentiated from meat-type chicken isolates. When compared to all meat-type isolates from China, Subgroup 1 exclusively contained current layer isolates and seemed to be dominant; all the isolates in this subgroup exhibited gene diversity, and many unique amino acid mutations were present. In contrast, the viruses in Subgroup 2 were perfectly conserved and shared high identity with the prototype meat-type chicken ALV-J strain HPRS-103. The two subgroups contained only two concurrent mutations at the same position. Moreover, most of the isolates in Subgroup 1 had two additional glycosylation sites (at positions 101 and 191) when compared with those in Subgroup 2. Our study provides evidence for the coexistence of two extremely different ALV-J subgroups in Chinese layers from 2008 to 2010, supporting the need for vaccine development and purification measures to prevent ALV-J infection in layers in China.     

Avian leukosis subgroup J in broiler breeders in Switzerland

Since a new envelope subgroup (J) of the avian leukosis-sarcomatosis-complex was isolated for the first time from broiler breeders in the United Kingdom in 1989 and was characterized and associated with myeloid leukosis (syn. myelocytomatosis) the emergence of this subgroup was reported from all over the world. Thus the first known case of subgroup J avian leukosis in Switzerland in four imported broiler breeder flocks will be described. A total of 53 broiler breeder birds from four flocks showing reduced performance and increased mortality were submitted for postmortem examination. Approximately 20 blood samples from each flock were monitored serologically for antibodies against avian leukosis virus subgroup J (ALV-J). On necropsy myeloid leukosis (ML) was diagnosed in all four flocks. Furthermore the blood samples of three flocks showed significant ELISA-titres for ALV-J.     

安徽省禽白血病感染的血清学调查及gp85基因的扩增

随机抽取安徽省3个肉种鸡场种鸡及3个地市农贸市场商品鸡的血清样本和泄殖腔拭子,采用ELISA进行鸡白血病检测,并对J亚群鸡白血病病毒抗体阳性鸡群中病鸡的肝组织、全血及上毒细胞提取DNA进行PCR扩增和基因测序。检测结果表明,3个肉种鸡场中J亚群鸡白血病抗体阳性检出率分别为：0、73.50%和15.22%;3个农贸市场商品鸡抗体阳性检出率分别为：12.00%、2.22%和9.10%。3个肉种鸡场A、B亚群鸡白血病的抗体阳性率分别为0、17.93%和1.08%,ALV抗原阳性率分别为2.17%、17.93%和15.22%。PCR检测结果表明,从可疑发病鸡的肝组织和全血中均能扩增出ALV-J gp85特异性片段。结果证实安徽省鸡群中有ALV-J感染,并呈不同程度的流行,应引起高度重视。     

The control of lymphoid leukosis in a flock White Plymouth Rock chickens

Summary Lymphoid leukosis (LL) was successfully controlled in a commercial basic breeding line of White Plymouth Rock chickens. The control method has been developed for breeder flocks and consists of three elements: - In the flock under study, homogenates of embryos from all eggs collected during a number of I4-day periods are tested for the presence of LL viruses. - Only eggs from hens that have been shown not to shed virus in their eggs are used for the production of progeny. The offspring are reared in isolation during the first two months of life, at which time the age-related resistance against tumour formation by LL viruses appears to be sufficiently developed. - The chickens are subsequently inoculated intramuscularly with LL viruses of subgroups A and B transferred to a conventional chicken house. The vaccination raises a solid immunity to horizontal LL virus exposure and, due to the age-related resistance, tumour formation does not follow. No excretion of LL viruses could be detected in three generations of White Plymouth Rock chickens to which the three elements of the control procedure were applied. Clinical disease was not observed in any of the chickens under notice.     

Differential expression of microRNAs in avian leukosis virus subgroup J-induced tumors

Avian leukosis virus subgroup J (ALV-J) has become pandemic and induced serious clinical outbreaks in chickens in China. In particular, ALV-J induced various clinical tumors in infected chickens, which caused enormous economic losses to poultry. In this study, an infectious clone from an epidemic ALV-J Chinese isolate designated HLJ09SH01 was constructed and rescued. The rescued virus (named rHLJ09SH01) was inoculated into specific-pathogen-free (SPF) layer chickens, and infected chickens were observed for 238 days to explore the oncogenicity of rHLJ09SH01. As a result, 57.9% of rHLJ09SH01-infected chickens produced tumors. Accumulating evidence shows that microRNAs (miRNAs) have a close relationship with tumorigenesis. To gain more insight into the tumorigenesis of ALV-J, a miRNA microarray was performed as part of an investigation of changes in host miRNA expression in a liver tumor from ALV-J infected chickens. The results showed that four miRNAs were significantly differentially expressed; these data were verified using real-time PCR. Bioinformatics analysis showed the differentially expressed miRNAs to be involved in some tumorigenesis-related signaling pathways, such as the MAPK signaling pathway and the Wnt signaling pathway, which may represent a possible signaling pathway that was involved in the ALV-J-induced tumorigenesis.     

安徽省五华鸡J亚群禽白血病的鉴定及其病理学观察

为调查安徽省五华鸡J亚群禽白血病(Avian leukosis virus subgroup J,ALV-J)的感染情况,采用ELISA对五华鸡进行P27抗原和ALV-J抗体检测.挑选5只抗原抗体阳性鸡进行PCR检测,同时将5只抗原抗体阳性鸡和5只抗原抗体阴性鸡进行剖检,制作病理切片.其中1只鸡PCR检测为阳性,能扩增出545 bp条带,PCR检测阳性的鸡其心脏有肿瘤、脾脏肿大等病理学变化;组织切片发现心脏、肝脏、脾、肾、肺等组织内有弥漫性髓细胞样瘤细胞或髓细胞瘤病灶,髓细胞样瘤细胞的细胞质内可见嗜酸性颗粒.结果表明五华鸡已经感染了ALV-J,且部分鸡个体已经发病.     

Pathogenicity of two recombinant avian leukosis viruses

We have recently described the isolation and molecular characteristics of two recombinant avian leukosis subgroup J viruses (ALV J) with an avian leukosis virus subgroup A envelope (r5701A and r6803A). In the present study, we examined the role of the subgroup A envelope in the pathogenesis of these recombinant viruses. Chickens of line 151(5) x 7(1) were inoculated at 1 day of age with r5701A, r6803A, Rous-associated virus type 1 (RAV-1), or strain ADOL-Hcl of ALV-J. At 2, 4, 10, 18, and 32 wk postinoculation (PI), chickens were tested for avian leukosis virus (ALV)-induced viremia, shedding, and neutralizing antibodies. All except one chicken inoculated with the recombinant viruses (98%) developed neutralizing antibodies by 10 wk PI compared with only 16% and 46% of the ADOL-Hcl and RAV-1-inoculated birds, respectively. ALV-induced tumors and mortality in the two groups inoculated with recombinant viruses were different. The incidence of tumors in groups inoculated with r5701A or RAV-1 was 100% compared with only 9% in the groups inoculated with r6803A or ADOL-Hcl. The data suggest that differences in pathogenicity between the two recombinant viruses might be due to differences in the sequence of the 3' untranslated region (presence or absence of the E element), and, therefore, not only the envelope but also other elements of the viral genome play an important role in the pathogenesis of ALV.