An Evaluation Of The Infection Status And Source Of Subgroup J Avian Leukosis Virus In Cloned Free-range Layers

Avian Leukosis is a disease caused by Avian Leukosis virus (ALV), which can give riseto all sorts of benign and malignant tumor. According to antigenicity of its envelope proteingp85related to host specificity, ALV has10subgroups of A to J, but chickens only can beinfected by subgroups A, B, C, D, E, and J. ALV-J was first isolated from commercialmeat-type chickens and has become one of the most common exogenous viruses among ALVs.In china, ALV-J occurred in province of Heilongjiang, Beijing, Jiangsu, Liaoning, Guangdong,Guangxi, Shanghai, Neimenggu, Shandong, Henan, and Ningxia. The mortality can reach upto30%～40%in some area. Besides, the disease has spread to local variety in our countrysuch as yellow broilers and hemp chickens, and did tremendous damages to poultry industry.Worse more, it brought the enormous challenge for breeds conservation and selection.30cloacal swabs were randomly collected from45-day-old cloned free-range layers tomeasure the p27antigen level by enzyme-linked immunosorbent assay (ELISA). In addition,6anticoagulant blood samples were aseptically collected at random from the flock when thelayers were60days old. These samples were centrifuged to obtain the leukocytes, which werethen used to inoculate chicken embryo fibroblast (CEF) cells for the identification of ALV-Jby indirect immunofluorescence (IFA). The flock’s production performance was alsoinvestigated, and10layers were necropsied to evaluate pathological changes at115days ofage. Paraffin-embedded sections of intumescent liver and spleen were prepared for antigenlocalisation using IFA. Among the cloacal swabs that were tested,87%(26/30) were positive.Of the blood samples tested,100%(6/6) were positive using IFA. Besides, the flock neverlaid eggs even though they reached the age of the first laying (110d). Furthermore, there werepathological changes present, including atrophy of the thymus and bursa of Fabricius,undeveloped ovaries, glandular stomach haemorrhage, and hepatosplenomegaly. Positivesignals were prevalent in paraffin-embedded sections of the intumescent liver and spleen.In the meantime, provirus DNA was extracted from4free-range layers, and2paternalparents (HR native cocks), and the gp85gene of ALV-J was amplified by PCR to analyse thegenetic variation. The results of the autogenous variation analysis showed that the6strainswere98.5%~99.7%homologous. This study indicated that there was persistent infection with ALV-J, which seriouslyreduced the production performance of the flock. In addition, the genetic variation analysisshowed that ALV-J in free-range layers was more likely to have originated from the paternalparent, the HR native cock.