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ARS Home » Southeast Area » Athens, Georgia » U.S. National Poultry Research Center » Endemic Poultry Viral Diseases Research » Research » Publications at this Location » Publication #369538

Research Project: Enhancing Genetic Resistance to Marek’s Disease in Poultry

Location: Endemic Poultry Viral Diseases Research

Title: Adiponectin and its receptor genes' expression in response to MDV infection of White Leghorns

item BAI, YING - Hebei University
item YUAN, PING - University Of Maryland
item Zhang, Huanmin
item RAMACHANDRAN, RAMESH - Pennsylvania State University
item YANG, NING - China Agricultural University
item SONG, JIUZHOU - University Of Maryland

Submitted to: Poultry Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 6/3/2020
Publication Date: 9/2/2020
Publication URL:
Citation: Bai, Y., Yuan, P., Luo, J., Zhang, H., Ramachandran, R., Miao, H., Yang, N., Song, J. 2020. Adiponectin and its receptor genes' expression in response to MDV infection of White Leghorns. Poultry Science. 99(9):4249-4258.

Interpretive Summary: Marek’s disease is an avian virus-induced disease in susceptible chicken, which continues to cost economic loss to the poultry industry. Advancement in MDV-infection induced biological changes in chicken would help better understand the viral infection and its subsequent impact, therefore, to facilitate better control measure of this disease in poultry. This study was designed to explore both RNA expression and protein translation levels of a few candidate genes known to relate to critical metabolic functions. The data from this study showed that one of the cytokine genes and a couple of receptor genes that facilitate this cytokine gene in important biological processes underwent varied alterations at both the message RNA level and the protein level in in different tissues in response to Marek’s virus infection. This finding also would improve the general understanding on lipid metabolism in response to herpesvirus infection.

Technical Abstract: Marek’s disease virus (MDV) causes T-cell lymphoma in susceptible chicken and is also related to an imbalance of the lipid metabolism. Adiponectin is a circulatory cytokine secreted from adipose tissue and exerts critical metabolic functions. Although the associations between adiponectin and diseases, including lipid disorder and noncardiac vascular diseases, have been reported, little is known about the relationship between MDV infection and adiponectin. Here, we challenged white Leghorns from Marek’s disease (MD)-susceptible and MD-resistant lines with MDV at 7 D of age and then explored the body weight and plasma lipoprotein levels at 21 D after MDV infection. Meanwhile, adiponectin and the expression of its receptors were detected using quantitative real-time PCR and Western blot. The results showed that MDV infection induced body weight loss in all the experimental birds. Meanwhile, the concentrations of total cholesterol and high-density lipoprotein were lower after the infection, although there was no significant difference (P > 0.05). However, the infection did not affect adiponectin circulating levels in plasma. MD-susceptible birds had much lower plasma adiponectin than MD-resistant birds (P < 0.01). In abdominal fat, there was no significant difference in adiponectin mRNA level. Still, we observed a significant decrease in adiponectin protein concentration, as well as adipoR1 and adipoR2, at both mRNA and protein levels in the infected compared with the noninfected MD-susceptible chickens. In the spleen, MDV infection significantly reduced the adiponectin mRNA expression but increased the protein in MD-susceptible chickens, which decreased both adipoR1 mRNA expression and protein levels. Also interestingly, the adipoR1 mRNA expression level was significantly increased in MD-susceptible chickens in the liver after MDV infection. All findings in the present study provided interesting insights into adiponectin metabolism in chickens after MDV infection, which helps to advance the understanding of lipid metabolism in response to herpesvirus infection.