文献类型： 外文期刊
作者： Goraya, Mohsan Ullah 1 ; Ziaghum, Fozia 3 ; Chen, Shilong 4 ; Raza, Ali 5 ; Chen, Ye 1 ; Chi, Xiaojuan 1 ;
作者机构： 1.Fujian Agr & Forestry Univ, Anim Sci Coll, Key Lab Fujian Taiwan Anim Pathogen Biol, Fuzhou 350002, Fujian, Peoples R China
2.Fujian Agr & Forestry Univ, Life Sci Coll, Fuzhou 350002, Fujian, Peoples R China
3.Bahauddin Zakariya Univ, Dept Pharm, Multan, Pakistan
4.Fujian Acad Agr Sci, Inst Anim Husb & Vet Med, Fuzhou 350002, Fujian, Peoples R China
5.Univ Queensland, Queensland Alliance Agr & Food Innovat, Brisbane, Qld 4072, Australia
关键词： Classical swine fever virus; Pathogenesis; Innate immunity; Immune evasion; Cellular immunity
期刊名称：MICROBIAL PATHOGENESIS （ 影响因子：3.738； 五年影响因子：3.663 ）
ISSN： 0882-4010
年卷期： 2018 年 119 卷
页码：
收录情况： SCI
摘要： Classical swine fever virus (CSFV) infection causes mild to severe diseases among pigs, depending on the age and immune status of the host and viral strains. CSFV targets various cells, including macrophages and conventional and plasmacytoid dendritic cells. Classical swine fever is one of the most devastating diseases of pigs which leads to high morbidity and mortality, and causes significant economic loss worldwide. In response to infection with CSFV, host innate immune system eliminates the virus by recognizing specific viral molecules via distinct cellular pattern recognition receptors. These receptors trigger downstream intracellular signaling pathways, which regulate the translocation and activation of transcription factors that control the production of cytokines and interferons (IFNs). In turn, these IFNs activate JAK-STAT signaling that governs the transcription of IFN-stimulated genes (ISGs) that play critical roles in antiviral immunity. However, CSFV has evolved different strategies to evade innate immune signaling and can establish persistent infection without being recognized by immune surveillance. In this review, we discuss the current understanding of host innate response to CSFV infection. We also summarize how CSFV evades innate immunity to establish its chronic infection.
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