Chikungunya virus (CHIKV) was first identified in 1952 as a causative agent of outbreaks. CHIKV is transmitted by two mosquito species, Aedes aegypti and A. albopictus. Symptoms after CHIKV infection in human are typically fever and joint pain, but can also include headache, muscle pain, joint swelling, polyarthralgia, and rash. CHIKV is an enveloped single-stranded, positive-sense RNA virus with a diameter of approximately 70 nm. The pathogenesis of CHIKV infection and the mechanism by which it evades the innate immune system remain poorly understood. Moreover, little is known about the roles of CHIKV-encoded genes in the viral evasion of host immune responses, especially type I interferon (IFN) responses. Therefore, in the present study, we screened CHIKV-encoded genes for their regulatory effect on the activation of nuclear factor kappa B (NF-κB), a critical transcription factor for the optimal activation of IFN-β. Among others, non-structural protein 2 (nsP2) strongly inhibited melanoma differentiation-associated protein 5 (MDA5)-mediated induction of the NF-κB pathway in a dose-dependent manner. Elucidation of the detailed mechanisms of nsP2 is anticipated to contribute to the development of virus-specific therapeutics against CHIKV infection.

中文翻译：

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基孔肯雅病毒 nsP2 损害 MDA5/RIG-I 介导的 NF-κB 启动子激活诱导：病毒特异性治疗的潜在靶标。

基孔肯雅病毒 (CHIKV) 于 1952 年首次被确定为爆发的病原体。CHIKV 由两种蚊子传播，埃及伊蚊和白纹伊蚊. 人类感染 CHIKV 后的症状通常是发烧和关节痛，但也可能包括头痛、肌肉痛、关节肿胀、多关节痛和皮疹。CHIKV 是一种有包膜的单链正链 RNA 病毒，直径约为 70 nm。CHIKV 感染的发病机制及其逃避先天免疫系统的机制仍知之甚少。此外，关于 CHIKV 编码基因在病毒逃避宿主免疫反应，尤其是 I 型干扰素 (IFN) 反应中的作用知之甚少。因此，在本研究中，我们筛选了 CHIKV 编码基因对核因子 kappa B (NF-κB) 激活的调节作用，NF-κB 是 IFN-β 最佳激活的关键转录因子。其中，非结构蛋白 2 (nsP2) 以剂量依赖性方式强烈抑制黑色素瘤分化相关蛋白 5 (MDA5) 介导的 NF-κB 通路诱导。阐明 nsP2 的详细机制有望有助于开发针对 CHIKV 感染的病毒特异性疗法。