Unité de Génétique Moléculaire des Bunyavirus, Paris, France.
Parasit Vectors. 2012 Nov 15;5:264. doi: 10.1186/1756-3305-5-264.
Arthropod-borne viral infections cause several emerging and resurging infectious diseases. Among the diseases caused by arboviruses, chikungunya is responsible for a high level of severe human disease worldwide. The salivary glands of mosquitoes are the last barrier before pathogen transmission.
We undertook a proteomic approach to characterize the key virus/vector interactions and host protein modifications that occur in the salivary glands that could be responsible for viral transmission by using quantitative two-dimensional electrophoresis.
We defined the protein modulations in the salivary glands of Aedes aegypti that were triggered 3 and 5 days after an oral infection (3 and 5 DPI) with chikungunya virus (CHIKV). Gel profile comparisons showed that CHIKV at 3 DPI modulated the level of 13 proteins, and at 5 DPI 20 proteins. The amount of 10 putatively secreted proteins was regulated at both time points. These proteins were implicated in blood-feeding or in immunity, but many have no known function. CHIKV also modulated the quantity of proteins involved in several metabolic pathways and in cell signalling.
Our study constitutes the first analysis of the protein response of Aedes aegypti salivary glands infected with CHIKV. We found that the differentially regulated proteins in response to viral infection include structural proteins and enzymes for several metabolic pathways. Some may favour virus survival, replication and transmission, suggesting a subversion of the insect cell metabolism by arboviruses. For example, proteins involved in blood-feeding such as the short D7, an adenosine deaminase and inosine-uridine preferring nucleoside hydrolase, may favour virus transmission by exerting an increased anti-inflammatory effect. This would allow the vector to bite without the bite being detected. Other proteins, like the anti-freeze protein, may support vector protection.
节肢动物传播的病毒感染可引起几种新发和再现传染病。在由虫媒病毒引起的疾病中,基孔肯雅热导致全球范围内严重人类疾病的发病率较高。蚊子的唾液腺是病原体传播前的最后一道屏障。
我们采用蛋白质组学方法来描述关键的病毒/载体相互作用和宿主蛋白修饰,这些作用和修饰可能导致基孔肯雅病毒(CHIKV)在经口感染后 3 天和 5 天(3 和 5 DPI)通过唾液腺传播。使用定量二维电泳进行了研究。
我们定义了埃及伊蚊唾液腺中的蛋白调制,这些蛋白调制是在经口感染基孔肯雅病毒(CHIKV)3 天和 5 天后(3 和 5 DPI)触发的。凝胶图谱比较显示,CHIKV 在 3 DPI 时调节了 13 种蛋白质的水平,而在 5 DPI 时调节了 20 种蛋白质的水平。两种时间点均调节了 10 种推定分泌蛋白的数量。这些蛋白质涉及吸血或免疫,但许多蛋白质尚无已知功能。CHIKV 还调节了参与几种代谢途径和细胞信号传导的蛋白质的数量。
我们的研究构成了对感染基孔肯雅病毒的埃及伊蚊唾液腺中蛋白质反应的首次分析。我们发现,对病毒感染的差异调节蛋白包括结构蛋白和几种代谢途径的酶。一些可能有利于病毒的存活、复制和传播,这表明虫媒病毒对昆虫细胞代谢的颠覆。例如,参与吸血的蛋白质,如短 D7、腺苷脱氨酶和肌苷-尿嘧啶偏爱核苷水解酶,可能通过发挥增强的抗炎作用来促进病毒的传播。这将允许向量在不被察觉的情况下叮咬。其他蛋白质,如抗冻蛋白,可能支持载体保护。