In our case, chickens were manifested with the symptom of enlarged liver and spleen, decreased egg production, together with lymphocyte infiltration in the portal vein periphlebitis. These signs are closely related with the description of BLS, which was caused by aHEV. Initially, we suspected whether the chickens were subjecting to aHEV infection. However, those clinical symptoms and lymphocyte infiltration are not specific in aHEV-affected chickens, they can also be observed in some other viral-caused diseases. Meanwhile, although we found edema, congestion and homogenous eosinophilic material in the liver cells, the necrosis was not seen in the histopathology, which was contradict with aHEV infection [14]. Together with the results of PCR and RT-PCR, we believe that ALV-J ought to be strongly associated with this syndrome.

In addition to this case, similar reports had occurred in many farms around China. Previously, we had detected the chickens with the same symptom like this case from different farms in Shandong Province and Guangxi Province (data not shown). Notably, only ALV-J was found in all these samples. Therefore, although we did not perform experiments in vivo to directly confirm that ALV-J contributes to hepatomegaly and splenomegaly, ALV-J infection should be closely associated with this syndrome. It deserves our attention that we did not find myelocytoma infiltration in the liver, indicating that hepatomegaly and splenomegaly was not caused by tumor cells. ALV-J might affect chicken liver and spleen through unknown mechanisms.

Previous studies about the tissue tropism of the ALV-J prototype strain HPRS-103 indicated that ALV-J can replicate well in most tissues. Although it does not directly induce tumors in some tissues, like liver and smooth muscle, ALV-J can alter the biological activities of the infected tissues [15]. Our previous research found that ALV-J replicated much faster in Leghorn male hepatoma (LMH) chicken liver cells than traditional DF-1 cells possible due to the high expression level of ALV-J receptor Na+/H+ exchanger type 1 (NHE1) in LMH cells [16]. It is also found that ALV-J can spontaneously and effectively induce the expression of NHE1 gene in primary chicken liver cells [17]. Both above indicate that the chicken liver is a perfect target for ALV-J infection. Further research in future is required to explore the relationship between ALV-J and liver cells.

Since it was first found in UK in 1989, ALV-J had undergone several significant mutations, together with different symptoms in clinic. ALV-J displays a high level of genetic variation and recombination, which posing the potential for the generation of novel strains with altered phenotypes in antigenicity, tissue tropism, host range and pathogenesis. Within the genomic RNA of ALV-J, env gene and 3’UTR are the most variable. Meanwhile, the two parts with mutations can greatly affect the viral pathogenicity. The env gene encodes the Env protein, which forms the outer layer of the virion and triggers the viral infection. Two highly variable regions in Env, hypervariable region 1 (hr1) and hypervariable region 2 (hr2), are responsible for the ligand–receptor interaction directly [18], while variable region 3 (vr3) recognizes the specific receptor [14]. The two ALV-J strains isolated in this study belong to the branch of layer chicken ALV-J isolates. However, JSYC2106-1 and JSYC2106-2 show only 90.3%-94.6% homology with other ALV-J strains in env gene.

r-TM and E element in the 3’UTR are two important factors which can affect the clinical symptoms directly. The r-TM is considered to be not a necessity for virus replication, but is linked to the pathogenicity of ALV-J in layer chickens [19]. E element is also dispensable for ALV-J, but it is closely related to the oncogenicity and viral replication in vivo [20]. E element also contributes to virus-encoded microRNAs [21]. Some early isolates, with a tact r-TM but without the E element, usually cause myeloma in broiler chicken. However, the layer chicken ALV-J isolates with a deletion of 205-bp in the r-TM and all E element can induce hemangioma. The two ALV-J strains JSYC2106-1 and JSYC2106-2 isolated here carry a complete E element, but with a deletion of 130bp in r-TM. It is possible that the two ALV-J strains with the unique 3’UTR might be as the intermediate between broiler and layer chicken ALV-J isolates. However, the pathogenesis of the two ALV-J isolates need to be further tested in vivo.

In summary, this report documented the detection and isolation of novel ALV-J in chicken flocks with the disease of hepatomegaly and splenomegaly, highlighting the closely relationship between ALV-J infection and chicken hepatomegaly and splenomegaly, and the significance of the ALV-J eradication program.

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