Abstract
Collagen triple helix repeat containing-1 (CTHRC1) has recently been identified as avian leukosis virus subgroup J (ALV-J) replication-dependent factor that remarkably facilitates ALV-J replication via interaction with the envelope glycoprotein (SU) of ALV-J. However, the dynamic distribution and localization of CTHRC1 in various tissues upon ALV-J infection are still unknown. In this study, data revealed that the levels of CTHRC1 were significantly increased in various tissues and that the protein was mainly located in the cytoplasm and nucleus of parenchymal cells in tissues of chickens that were infected by ALV-J naturally and experimentally. Interestingly, CTHRC1 was also observed in leukocytes other than erythrocytes in congested veins of ALV-J-infected tissues. Consequently, the positive cells in these veins were confirmed as lymphocytes by laser confocal microscopy. Taken together, these results conclude that the CTHRC1 is an inducible protein and exhibited ubiquitous expression in ALV-J-infected chickens, which may provide basic information for in-depth study of ALV-J infection and replication mechanisms.
Highlights
Avian leukosis virus subgroups (ALVs) belonging to type C retroviruses are generally divided into seven subgroups (A–E, J, and K) [1,2,3]
In order to further clarify that Collagen triple helix repeat containing-1 (CTHRC1) is an inducible protein upon avian leukosis virus subgroup J (ALV-J) infection, we inoculated the virus of isolated into DF-1 cells and tested whether ALV-J up-regulated the expression of CTHRC1
The results showed that CTHRC1 was elevated upon ALV-J infection (Figures 1B,C)
Summary
Avian leukosis virus subgroups (ALVs) belonging to type C retroviruses are generally divided into seven subgroups (A–E, J, and K) [1,2,3]. It is noteworthy that since isolation of the first strain (HPRS-103) from meat-type chickens in the United Kingdom in the late 1980s, more attention has been focused on the J subgroup of ALV (ALV-J), which caused high mortality, wide host ranges, and strong tumorigenicity [4, 5]. Attributed to the implementation of ALV-J eradication program [6], there were rarely reports of ALV-J or myelocytomatosis in China after 2013. There were another intensive reports about ALV-J breakout almost simultaneously in six provinces of China in 2018, which attracted our attention [7]. It is rather remarkable that there were extensive medullary-like tumor cells in the bone marrow, liver, and kidney, and all of the neoplasms were myelocytomas [7]
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