Antibody-dependent enhancement of PRRSV infection down-modulates TNF-alpha and IFN-beta transcription in macrophages
文献类型: 外文期刊
第一作者: Bao, Dengke
作者: Bao, Dengke;Wan, Bo;Wang, Yinbiao;Zhang, Gaiping;Bao, Dengke;Wang, Rui;Qiao, Songlin;Wan, Bo;Wang, Yinbiao;Liu, Mingyang;Shi, Xibao;Guo, Juiqing;Zhang, Gaiping
作者机构:
关键词: Porcine reproductive and respiratory syndrome virus (PRRSV);Antibody-dependent enhancement (ADE);FcγRIIb;Interferon;Down-modulate
期刊名称:VETERINARY IMMUNOLOGY AND IMMUNOPATHOLOGY ( 影响因子:2.046; 五年影响因子:2.217 )
ISSN:
年卷期:
页码:
收录情况: SCI
摘要: Porcine reproductive and respiratory syndrome (PRRS) is an infectious disease, resulting in important economic losses in pig farming. Previous studies have shown that Fey receptor (Fc gamma R)-mediated entry of infectious PRRSV immune complexes into macrophages plays a pivotal role in the pathogenesis of the disease. This study demonstrates that PRRSV was able to suppress the transcription of key antiviral genes tumor necrosis factor-alpha (TNF-alpha) and interferon-beta (IFN-beta), when infection was via the ADE pathway. Investigation of this infection pathway found that PRRSV suppresses the antiviral genes by disrupting the transcription of the genes coding for the associated transcription factors interferon regulatory factor-1 (IRF-1), interferon regulatory factor-3 (IRF-3) and nuclear factor kappa B (NF-kappa B). The ADE pathway of infection allows PRRSV to specifically target antiviral genes and alters the innate intracellular immune responses in macrophages. The ADE mechanism described in this study furthers our understanding of pathogenesis following PRRSV infection and is of general relevance to virally induced disease and in relation to antiviral vaccination strategies
分类号: S85
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