先天免疫系统
猪瘟
生物
免疫学
免疫系统
免疫
病毒
模式识别受体
获得性免疫系统
病毒学
作者
Mohsan Ullah Goraya,Fozia Ziaghum,Shilong Chen,Ali Raza,Ye Chen,Xiaojuan Chi
标识
DOI:10.1016/j.micpath.2018.04.020
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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