Host lipid metabolism influences the variation in resistance of Pekin ducks to duck hepatitis A virus genotype 3

被引:0
作者
Liang, Suyun [1 ]
Chang, Zhuo [2 ]
Lu, Meixi [1 ]
Guo, Zhanbao [1 ]
Luo, Dawei [1 ]
Xing, Guangnan [1 ]
Xie, Ming [1 ]
Huang, Wei [1 ]
Hou, Shuisheng [1 ]
机构
[1] Chinese Acad Agr Sci, Inst Anim Sci, 2 Yuanmingyuan West Rd, Beijing 100193, Peoples R China
[2] Beijing Gen Stn Anim Husb, Beijing 100107, Peoples R China
关键词
DHAV-3; Lipid metabolism; Pekin duck; CHOLESTEROL; PHOSPHATIDYLSERINE; EXPRESSION; INFECTION; SEROTYPE;
D O I
10.1016/j.ijbiomac.2024.139168
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Duck viral hepatitis (DVH) is a common and serious acute infectious disease that has a significantly impact on the duck farming industry. Duck hepatitis A virus type 3 (DHAV-3) is the major causative agent of DVH in East Asia. Host factor indicators of resistance to DHAV-3 in Pekin ducks were investigated using resistant (Z7R) and susceptible (Z7S) duck lines. Before DHAV-3 infection, Z7R had significantly higher HDL-C and LDL-C levels than Z7S. The results of population verification showed that Pekin ducks with HDL-C and/or LDL-C concentrations within their maximum 5 % confidence interval were highly resistant to DHAV-3. RNA-seq identified fifteen differentially expressed genes, primarily involved in lipid metabolism. Additionally, lipidomics identified one hundred distinct metabolites involved in glycerophospholipid metabolism. The ACSL6 gene was found to be significantly associated with PC and PE. ACSL6, PE, PC, HDL-C and LDL-C co-regulated hepatic lipid metabolism. In conclusion, our results reveal that HDL-C and LDL-C may serve as markers of anti-DHAV-3 infection and lipid metabolism may be related to a potential mechanism of antiviral activity in Pekin ducks, providing a theoretical basis for future studies on the interaction between lipid metabolism and DHAV-3.
引用
收藏
页数:10
相关论文
共 57 条
[11]   Glutathione: Overview of its protective roles, measurement, and biosynthesis [J].
Forman, Henry Jay ;
Zhang, Hongqiao ;
Rinna, Alessandra .
MOLECULAR ASPECTS OF MEDICINE, 2009, 30 (1-2) :1-12
[12]   Molecular detection and typing of duck hepatitis A virus directly from clinical specimens [J].
Fu, Yu ;
Pan, Meng ;
Wang, Xiaoyan ;
Xu, Yongliang ;
Yang, Hanchun ;
Zhang, Dabing .
VETERINARY MICROBIOLOGY, 2008, 131 (3-4) :247-257
[13]   Lipid Abnormalities and Inflammation in HIV Inflection [J].
Funderburg, Nicholas T. ;
Mehta, Nehal N. .
CURRENT HIV/AIDS REPORTS, 2016, 13 (04) :218-225
[14]   Increased Expression of LDL Receptor-Related Protein 1 during Human Cytomegalovirus Infection Reduces Virion Cholesterol and Infectivity [J].
Gudleski-O'Regan, Nicole ;
Greco, Todd M. ;
Cristea, Ileana M. ;
Shenk, Thomas .
CELL HOST & MICROBE, 2012, 12 (01) :86-96
[15]   INVITRO ISOLATION, PROPAGATION, AND CHARACTERIZATION OF DUCK HEPATITIS-VIRUS TYPE-III [J].
HAIDER, SA ;
CALNEK, BW .
AVIAN DISEASES, 1979, 23 (03) :715-729
[16]   Viruses 'chew the fat'!? [J].
Hertzog, Paul .
IMMUNOLOGY AND CELL BIOLOGY, 2014, 92 (02) :100-102
[17]  
Kim D, 2015, NAT METHODS, V12, P357, DOI [10.1038/NMETH.3317, 10.1038/nmeth.3317]
[18]   Recent Korean isolates of duck hepatitis virus reveal the presence of a new geno- and serotype when compared to duck hepatitis virus type 1 type strains [J].
Kim, M.-C. ;
Kwon, Y.-K. ;
Joh, S.-J. ;
Kim, S.-J. ;
Tolf, C. ;
Kim, J.-H. ;
Sung, H.-W. ;
Lindberg, A. M. ;
Kwon, J.-H. .
ARCHIVES OF VIROLOGY, 2007, 152 (11) :2059-2072
[19]  
LANDINI MP, 1984, J GEN VIROL, V65, P1229, DOI 10.1099/0022-1317-65-7-1229
[20]   Chewing the Fat: The Conserved Ability of DNA Viruses to Hijack Cellular Lipid Metabolism [J].
Lange, Philip T. ;
Lagunoff, Michael ;
Tarakanova, Vera L. .
VIRUSES-BASEL, 2019, 11 (02)