[1]BILODEAU R, DEA S, SAUVAGEAU R A, et al. Porcine reproductive and respiratory syndrome′ in Quebec [J]. Vet Rec, 1991, 129(5): 102-103.
[2]ALBINA E. Epidemiology of porcine reproductive and respiratory syndrome (PRRS): an overview [J]. Vet Microbiol, 1997, 55 (1-4): 309-316.
[3]ZHOU L, YANG H. Porcine reproductive and respiratory syndrome in China [J]. Virus Res, 2010, 154 (1-2): 31-37.
[4]LI Y, WANG X, BO K, et al. Emergence of a highly pathogenic porcine reproductive and respiratory syndrome virus in the Mid-Eastern region of China [J]. Vet J, 2007, 174(3): 577-584.
[5]TIAN K, YU X, ZHAO T, et al. Emergence of fatal PRRSV variants: unparalleled outbreaks of atypical PRRS in China and molecular dissection of the unique hallmark [J]. PLoS One, 2007, 2(6): e526.
[6]TONG G Z, ZHOU Y J, HAO X F, et al. Highly pathogenic porcine reproductive and respiratory syndrome, China [J]. Emerg Infect Dis, 2007, 13(9): 1434-1436.
[7]杨汉春,周磊. 猪繁殖与呼吸综合征病毒的遗传变异与演化 [J]. 生命科学, 2016, 28(3): 325-336.
YANG H C, ZHOU L. Genetic variation and evolution of porcine reproductive and respiratory syndrome virus [J]. Chinese Bulletin of Life Sciences, 2016, 28(3): 325-336. (in Chinese)
[8]胡景杰,郭鑫,李人卫,等. 畜禽重要病原的致病机理研究——国家自然科学基金重大项目介绍 [J]. 畜牧兽医学报,2014, 45(12): 2088-2090.
HU J J, GUO X,LI R W,et al. Pathogenesis study of important pathogens in livestock and poultry: an introduction to a major project of National Natural Science Foundation of China [J]. Acta Veterinaria et Zootechnica Sinica, 2014, 45(12): 2088-2090. (in Chinese)
[9]ZHOU L, ZHANG J, ZENG J, et al. The 30-amino-acid deletion in the Nsp2 of highly pathogenic porcine reproductive and respiratory syndrome virus emerging in China is not related to its virulence [J]. J Virol, 2009, 83(10): 5156-5167.
[10]LI Y, ZHOU L, ZHANG J, et al. Nsp9 and Nsp10 contribute to the fatal virulence of highly pathogenic porcine reproductive and respiratory syndrome virus emerging in China [J]. PLoS Pathog, 2014, 10 (7): e1004216.
[11]WEI Z, LIN T, SUN L, et al. N-linked glycosylation of GP5 of porcine reproductive and respiratory syndrome virus is critically important for virus replication in vivo [J]. J Virol, 2012, 86(18): 9941-9951.
[12]LUO R, XIAO S, JIANG Y, et al. Porcine reproductive and respiratory syndrome virus (PRRSV) suppresses interferon-beta production by interfering with the RIG-I signaling pathway [J]. Mol Immunol, 2008, 45(10): 2839-2846.
[13]SHI Y, LI Y, LEI Y, et al. A dimerization-dependent mechanism drives the endoribonuclease function of porcine reproductive and respiratory syndrome virus nsp11 [J]. J Virol, 2016, 90(9): 4579-4592.
[14]XIAO S, WANG X, NI H, et al. MicroRNA miR-24-3p promotes porcine reproductive and respiratory syndrome virus replication through suppression of heme oxygenase-1 expression [J]. J Virol, 2015, 89 (8): 4494-4503.
[15]GAO L, GUO X K, WANG L, et al. MicroRNA 181 suppresses porcine reproductive and respiratory syndrome virus (PRRSV) infection by targeting PRRSV receptor CD163 [J]. J Virol, 2013, 87(15): 8808-8812.
[16]GUO X K, ZHANG Q, GAO L, et al. Increasing expression of microRNA 181 inhibits porcine reproductive and respiratory syndrome virus replication and has implications for controlling virus infection [J]. J Virol, 2013, 87(2): 1159-1171.
[17]FU Y, QUAN R, ZHANG H, et al. Porcine reproductive and respiratory syndrome virus induces interleukin-15 through the NF-κB signaling pathway [J]. J Virol, 2012, 86(14): 7625-7636.
[18]HU Y, CONG X, CHEN L, et al. Synergy of TLR3 and 7 ligands significantly enhances function of DCs to present inactivated PRRSV antigen through TRIF/MyD88-NF-κB signaling pathway [J]. Sci Rep, 2016, 6: 23977. |