|Li, Hongmei -|
|Ji, Jun -|
|Xie, Qingmei -|
|Shang, Huiqin -|
|Xin, Xuegang -|
|Chen, Feng -|
|Sun, Baoli -|
Submitted to: Virus Research
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: July 4, 2012
Publication Date: July 16, 2012
Repository URL: http://handle.nal.usda.gov/10113/56452
Citation: Li, H., Yji, J., Xie, Q., Shang, H., Zhang, H., Xin, X., Chen, F., Sun, B. 2012. Aberrant expression of liver microRNA in chickens infected with subgroup J avian leukosis virus. Virus Research. 169(2012):268-271. Available: http://dx.doi.org/10.1016/j.virusres.2012.07.003. Interpretive Summary: Subgroup J avian leukosis virus (ALV-J) is an oncogenic retrovirus that causes myeloid leukosis, a cancer-like disease, found primarily in meat-type of chickens. Although ALV-J infection is well under control in the U.S.A., ALV-J outbreaks occur in other parts of the world each year; such outbreaks constitute a threat to the prosperity of the world's poultry industry, and create trade barriers for the world market. To explore genetic factors that influence ALV-J infected chickens, we examined the expression of some host molecular genetic componetes named microRNAs, a class of small RNA molecules about 22 nucleotides each in length, in ALV-J infected and uninfected chickens. A dozen of microRNAs were found for the first time in the liver of ALV-J-infected chickens. The numbers of the microRNAs were significantly different from that noted in uninfected chickens. This finding paves the way for further exploration of genetic factors that may control or influence ALV-J infection and subsequent disease outcomes.
Technical Abstract: Subgroup J avian leukosis virus (ALV-J) is an oncogenic retrovirus primarily causing myeloid leukosis (ML) in broilers. Although ALV is well under control in a few countries including the U.S.A., poultry industry in many parts of the world continues suffering from serious economic loss due to sporadic or widespread ALV infection, especially ALV-J infection. ALV-J infection of chickens is reportedly mediated by a cellular receptor. So far, however, no genetic variant of the receptor gene that confers resistance to ALV-J has been identified. To advance our understanding on epigenetic factors that are involved in the event of ALV-J infection, we examined the expression of miRNAs in livers of 10-week-old chickens uninfected or infected with ALV-J by miRNA microarray analysis. Our data showed there were 12 miRNAs differentially expressed in liver between the uninfected and infected groups (P < 0.01). Of which, the expressions of seven miRNAs (gga-mir-221, gga-mir-222, gga-mir-1456, gga-mir-1704, gga-mir-1777, gga-mir-1790, and gga-mir-2127,) were upregulated by ALV-J infection and may be involved in oncogenicity. The other five miRNAs (gga-let-7b, gga-let-7i, gga-mir-125b, gga-mir-375, and gga-mir-458) were significantly downregulated. The downregulated miRNAs may play important roles in tumor suppression. This finding paves the way for further exploration of epigenetic influence on tumorigenicity upon ALV-J infection.