Shi Zuo-Kun, Wen Dan, Chang Meng-Meng, Sun Xiao-Mei, Wang Yan-Hong, Cheng Chi-Hang, Zhang Li-Qin, Zheng Ai-Hua, Zou Zhen
State Key Laboratory of Integrated Management of Pest Insects and Rodents, Institute of Zoology, Chinese Academy of Sciences, Beijing, China.
CAS Center for Excellence in Biotic Interactions, University of Chinese Academy of Sciences, Beijing, China.
mSystems. 2021 Jun 29;6(3):e0119020. doi: 10.1128/mSystems.01190-20. Epub 2021 May 26.
Zika virus (ZIKV; ) is a devastating virus transmitted to humans by the mosquito Aedes aegypti. The interaction of the virus with the mosquito vector is poorly known. The double-stranded RNA (dsRNA)-mediated interruption or activation of immunity-related genes in the Toll, IMD, JAK-STAT, and short interfering RNA (siRNA) pathways did not affect ZIKV infection in A. aegypti. Transcriptome-based analysis indicated that most immunity-related genes were upregulated in response to ZIKV infection, including leucine-rich immune protein (LRIM) genes. Further, there was a significant increment in the ZIKV load in , , and -silenced A. aegypti, suggesting their function in modulating viral infection. Further, gene function enrichment analysis revealed that viral infection increased global ribosomal activity. Silencing of and , two ribosomal large subunit genes, increased mosquito resistance to ZIKV infection. fat body culture assay revealed that the expression of and was responsive to the Juvenile hormone (JH) signaling pathway. These two genes were transcriptionally regulated by JH and its receptor methoprene-tolerant (Met) complex. Silencing of also inhibited ZIKV infection in A. aegypti. This suggests that ZIKV enhances ribosomal activity through JH regulation to promote infection in mosquitoes. Together, these data reveal A. aegypti immune responses to ZIKV and suggest a control strategy that reduces ZIKV transmission by modulating host factors. Most flaviviruses are transmitted between hosts by arthropod vectors such as mosquitoes. Since therapeutics or vaccines are lacking for most mosquito-borne diseases, reducing the mosquito vector competence is an effective way to decrease disease burden. We used high-throughput sequencing technology to study the interaction between mosquito Aedes aegypti and ZIKV. Leucine-rich immune protein (LRIM) genes were involved in the defense in response to viral infection. In addition, RNA interference (RNAi) silencing of and , two JH-regulated ribosomal large subunit genes, suppressed ZIKV infection in A. aegypti. These results suggest a novel control strategy that could block the transmission of ZIKV.
寨卡病毒（ZIKV）是一种通过埃及伊蚊传播给人类的毁灭性病毒。人们对该病毒与蚊虫媒介之间的相互作用了解甚少。双链RNA（dsRNA）介导的Toll、IMD、JAK - STAT和小干扰RNA（siRNA）途径中免疫相关基因的中断或激活，并不影响埃及伊蚊中的寨卡病毒感染。基于转录组的分析表明，大多数免疫相关基因在寨卡病毒感染后上调，包括富含亮氨酸的免疫蛋白（LRIM）基因。此外，LRIM1、LRIM2和APL1C基因沉默的埃及伊蚊中寨卡病毒载量显著增加，表明它们在调节病毒感染中发挥作用。此外，基因功能富集分析显示病毒感染增加了整体核糖体活性。核糖体大亚基基因RPL11和RPL13沉默后，增强了蚊虫对寨卡病毒感染的抗性。脂肪体培养试验表明，RPL11和RPL13的表达对保幼激素（JH）信号通路有反应。这两个基因受JH及其受体耐甲氧普烯（Met）复合物的转录调控。RPL13沉默也抑制了埃及伊蚊中的寨卡病毒感染。这表明寨卡病毒通过JH调节增强核糖体活性，以促进在蚊虫中的感染。总之，这些数据揭示了埃及伊蚊对寨卡病毒的免疫反应，并提出了一种通过调节宿主因子来减少寨卡病毒传播的控制策略。大多数黄病毒通过蚊虫等节肢动物媒介在宿主之间传播。由于大多数蚊媒疾病缺乏治疗方法或疫苗，降低蚊虫媒介能力是减轻疾病负担的有效途径。我们使用高通量测序技术研究埃及伊蚊与寨卡病毒之间的相互作用。富含亮氨酸的免疫蛋白（LRIM）基因参与了对病毒感染的防御反应。此外，JH调节的两个核糖体大亚基基因RPL11和RPL13的RNA干扰（RNAi）沉默抑制了埃及伊蚊中的寨卡病毒感染。这些结果提示了一种可以阻断寨卡病毒传播的新型控制策略。
