登革热病毒发病机制的综合观点
摘要
体依赖性增强（ADE）、记忆交叉反应性T细胞、抗DENV NS1抗体、自身免疫以及遗传因素是疾病易感性的主要决
定因素。NS1蛋白和抗DENV NS1抗体被认为是导致严重登革热发病机制的原因。交叉反应性CD4 T细胞的细胞
因子反应可能会因不同DENV血清型的连续感染而改变，导致促炎细胞因子进一步升高，从而导致有害的免疫反应。
Fcγ受体介导的抗体依赖性增强（ADE）导致免疫细胞释放细胞因子，导致血管内皮细胞功能障碍和血管通透性增
加。登革热病毒的基因组变异和抑制宿主免疫反应的亚基因组黄病毒RNA（sfRNA）是疾病严重程度的病毒决定因
素。登革热感染可导致产生针对DENV NS1抗原、DENV prM和E蛋白的自身抗体，这些抗体可以与多种自身抗原
如纤溶酶原、整合素和血小板细胞发生交叉反应。除了病毒因素外，一些宿主遗传因素和基因多态性也在DENV感
染的发病机制中发挥作用。这篇综述文章强调了导致登革热发病机制的各种因素，并强调了与生物标志物相关的领
域的最新进展，这些标志物可用于预测严重的疾病结果。
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[1]Mutheneni SR, Morse AP, Caminade C, Upadhyayula
SM. Dengue burden in India: recent trends and importance of
climatic parameters. Emerg Microbes Infect. 2017;6(8):e70.
[2]Hussain T, Jamal M, Rehman T, Andleeb S. Dengue:
pathogenesis, prevention and treatment – a mini review. Adv
Life Sci. 2015;2(3):110–114.
[3]Mustafa MS, Rasotgi V, Jain S, Gupta V. Discovery
of fifth serotype of dengue virus (DENV-5): a new public
health dilemma in dengue control. Med J Armed Forces India.
2015;71(1):67–70.
[4]Chaturvedi UC, Agarwal R, Elbishbishi EA,
Mustafa AS. Cytokine cascade in dengue hemorrhagic fever:
implications for pathogenesis. FEMS Immunol Med Microbiol.
2000;28(3):183–188.
[5]An, J., D. S. Zhou, J. L. Zhang, H. Morida, J. L. Wang,
and K. Yasui. 2004. Dengue-specific CD8+ T cells have both
protective and pathogenic roles in dengue virus infection.
Immunol. Lett. 95:167-174.
[6]Atrasheuskaya, A., P. Petzelbauer, T. M. Fredeking,
and G. Ignatyev. 2003. Anti-TNF antibody treatment reduces
mortality in experimental dengue virus infection. FEMS
Immunol. Med. Microbiol. 35:33-42.
[7]Avirutnan, P., L. Zhang, N. Punyadee, A. Manuyakorn,
C. Puttikhunt, W. Kasinrerk, P. Malasit, J. P. Atkinson, and
M. S. Diamond. 2007. Secreted NS1 of dengue virus attaches
to the surface of cells via interactions with heparan sulfate and
chondroitin sulfate E. PLoS Pathog. 3:e183.
[8]Atrasheuskaya, A., P. Petzelbauer, T. M. Fredeking,
and G. Ignatyev. 2003. Anti-TNF antibody treatment reduces
mortality in experimental dengue virus infection. FEMS
Immunol. Med. Microbiol. 35:33-42.
[9]Guzman MG, Alvarez M, Halstead SB. Secondary
infection as a risk factor for dengue hemorrhagic fever/
dengue shock syndrome: an historical perspective and role of
antibody-dependent enhancement of infection. Arch Virol.
2013;158(7):1445–1459.
[10]Aoki, S., M. Osada, M. Kaneko, Y. Ozaki, and Y.
Yatomi. 2007. Fluid shear stress enhances the sphingosine
1-phosphate responses in cell-cell interactions between
platelets and endothelial cells. Biochem. Biophys. Res.
Commun. 358:1054-1057.
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