Dynamics Of Avian Leukosis Virus And Pathology Of Avian Leukosis In Egg-type Chickens

The avian leukosis/sarcoma viruses are retroviruses which induce a variety of benign and malignant neoplasms in the domestic fowl. To make clear about dynamics of antibodies and the pathological mechanism of Avian Leukosis Virus (ALV), the infection states of ALV and pathology of Avian Leukosis (AL) were studied in two egg-type flocks which had been infected with more than one type virus.This study consists of three sections: the first one is the detection of the antibodies of ALVs subgroup A/B and J, and the antigen of ALVs p27. 4 parent chickens with the positive antibody of ALV-J and ALV-A/B were selected and producted 21 commercial chickens. The antibody and antigen of ALV were detected for 40 weeks. The results showed that the co-infection of ALV-J and ALV-A/B had existed in this breed flock. The antibodies of ALV-J and ALV-A/B could not only co-exist but also have the ability to promote each other's development in the same chicken. The antibody level of ALV-J and ALV-A/B was relatively high in the parent ones, however, the co-infection of ALV-J and ALV-A/B was not detected in the commercial ones. In the second section, histopathological examination was done to chickens displaying clinical manifestation. Sick birds showed the enlargement of livers, with white nodules on the surface. Spleens and kidneys displayed slight enlargement also. Myelocytoma cells with reddish granules in the cytoplasm distributed in the white pulp of spleen. In heart, normal cardiomyocytests were squeezed or even occupied by tumour cells. Lymphosarcoma cells were the majority, and myelocytoma cells distributed in normal tissues. There were a lot of nodules which were consisted of myelocytoma cells in lung. White noduls distributed in livers, and the majority of which were lymphosarcoma cells. Tumour cells distributed in hepatic lobules and around the blood vessels, and the normal structure of liver was destroyed. There were a majority of lymphosarcoma cells between renal tubulars. Proventriculus'interstitial extension was obvious, in which there were a lot of lymphosarcoma cells. Two types of tumour cells, lymphosarcoma cells and myelocytoma cells, were observed in the same section, which indicated that the co-infection of ALV-J and ALV-A/B could induced different tumour cells as their target cells. In the third experiment, virus isolation and identification, the analysis of genetic evolution process and pathology observation were conducted from egg-type chickens with proventriculitis. The results indicated that ALV-J was isolated form 9 laying hens, and co-infection of ALV-J with reticuloendotheliosis virus was also confirmed in 4 chickens. The expected results were obtained from PCR. Sequence comparisons indicated that the provetriculus isolate had 97.8% identity with the HPPS103 strain isolated from white meat-type chickens and 93.0% identity with SD07LK1 strain from egg-type chickens. The gross pathology of ten chickens was similar, which showed comb pallor. Proventriculus showed 2 to 3 times enlargement compared with normal ones, and the purulent exudate were observed from the nearly disappeared gastric glands. A lot of lymphocytes were seen in normal structure of proventriculus. Viruses, with the diameter about 60nm to 90nm, were observed in these cases. Lymphocytes in proventriculus were deformed and the normal structure changed. The membrane of nuclear, mitochondria and cytoplasma and most organelles were dissolved. Many vacuoles emerged in cytoplasm and it was hardly to discern the outline of mitochondrias which were showed hydropic degeneration. The number increase of lymphocytes and hydropic degeneration in and between cells might be responsible for the enlargement of proventriculus.In conclusion, the co-infection of viruses should be responsible for the outbreak of AL in egg-type flocks in recent years, which special attention should be given in poultry industry nowadays.