Cytokines Disregulation in Birds and Mammals Infected by Avian Influenza Virus

IF 0.3
D. Hewajuli, N. Dharmayanti
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引用次数: 1

Abstract

Highly Pathogenic Avian Influenza (HPAI) virus causes severe dysfunction in nervous system lead to mortality in birds and mammals. The innate immunity plays an important role as initial barrier against the infection that stimulated by recognition of pathogens through Toll like Receptor (TLR). TLR activates Nuclear Factor-kappa B cascade pathway. Cytokines are mediators to initiate, proliferate and regulate inflammation against the virus infection. They are classified according to their activities or target cells, such as interferons, interleukins, chemokines, colony stimulating factor, and tumor necrosis factors. The gene expression of cytokine was found in different organs of chicken and mammals infected with HPAI and Low Pathogenic Avian Influenza (LPAI) virus to express immune response against infection. The HPAI and LPAI viruses cause up-regulated and down-regulated cytokines, disruption of cell mediated immune response lead to increased AI virus pathogenicity. The objective of this review is to describe disregulation mechanism of cytokines that increase AI virus pathogenicity in birds and mammals.
禽流感病毒感染的鸟类和哺乳动物细胞因子失调
高致病性禽流感(HPAI)病毒在鸟类和哺乳动物中引起严重的神经系统功能障碍,导致死亡。先天免疫通过Toll样受体(Toll like Receptor, TLR)对病原体进行识别,作为机体抵抗感染的初始屏障,发挥着重要作用。TLR激活核因子- κ B级联通路。细胞因子是启动、增殖和调节对抗病毒感染的炎症的介质。根据其活性或靶细胞进行分类,如干扰素、白细胞介素、趋化因子、集落刺激因子、肿瘤坏死因子等。在感染高致病性禽流感(HPAI)和低致病性禽流感(LPAI)病毒的鸡和哺乳动物的不同器官中发现了细胞因子的基因表达,表达对感染的免疫应答。高致病性禽流感病毒和低致病性禽流感病毒引起细胞因子上调和下调,破坏细胞介导的免疫反应导致病毒致病性增加。这篇综述的目的是描述细胞因子的失调机制,增加禽流感病毒在鸟类和哺乳动物的致病性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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16 weeks
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