Genetic characterization of bovine viral diarrhea virus strains in Beijing, China and innate immune responses of peripheral blood mononuclear cells in persistently infected dairy cattle

被引:20
作者
Weng, Xiao Gang [1 ]
Song, Quan Jiang [1 ]
Wu, Qiong [1 ]
Liu, Ming Chao [1 ]
Wang, Meng Ling [1 ]
Wang, Jiu Feng [1 ]
机构
[1] China Agr Univ, Coll Vet Med, Beijing 100193, Peoples R China
关键词
bovine viral diarrhea virus; interferon regulatory factor; persistent infection; phylogenetic analysis; Toll-like receptor; DENDRITIC CELLS; ANTIVIRAL RESPONSE; INTERFERON; IDENTIFICATION; SUBGENOTYPES; PREVALENCE; ACTIVATION; INDUCTION; EFFECTORS; HERDS;
D O I
10.4142/jvs.2015.16.4.491
中图分类号
S85 [动物医学(兽医学)];
学科分类号
0906 ;
摘要
To acquire epidemiological data on the bovine viral diarrhea virus (BVDV) and identify cattle persistently infected (PI) with this virus, 4,327 samples from Holstein dairy cows were screened over a four-year period in Beijing, China. Eighteen BVD viruses were isolated, 12 from PI cattle. Based on genetic analysis of their 5'-untranslated region (5'-UTR), the 18 isolates were assigned to subgenotype BVDV-1m, 1a, 1d, 1q, and 1b. To investigate the innate immune responses in the peripheral-blood mononuclear cells of PI cattle, the expression of Toll-like receptors (TLRs), RIG-I-like receptors, interferon-alpha (IFN-beta), IFN-beta, myxovirus (influenza virus) resistance 1 (MX1), and interferon stimulatory gene 15 (ISG15) was assessed by qPCR. When compared with healthy cattle, the expression of TLR-7, IFN-alpha, and IFN-beta mRNA was downregulated, but the expression of MX1 and ISG-15 mRNA was upregulated in PI cattle. Immunoblotting analysis revealed that the expression of interferon regulatory factor 3 (IRF-3) and IRF-7 was lower in PI cattle than in healthy cattle. Thus, BVDV-1m and la are the predominant subgenotypes in the Beijing region, and the strains are highly divergent. Our findings also suggest that the TLR-7/IRF-7 signaling pathway plays a role in evasion of host restriction by BVDV.
引用
收藏
页码:491 / 500
页数:10
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