State Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing 100071, China.
Viruses. 2021 Feb 22;13(2):343. doi: 10.3390/v13020343.
Dengue virus (DENV), a member of the genus of the Flaviviridae family, can cause dengue fever (DF) and more serious diseases and thus imposes a heavy burden worldwide. As the main vector of DENV, mosquitoes are a serious hazard. After infection, they induce a complex host-pathogen interaction mechanism. Our goal is to further study the interaction mechanism of viruses in homologous, sensitive, and repeatable C6/36 cell vectors. Transcriptome sequencing (RNA-Seq) technology was applied to the host transcript profiles of C6/36 cells infected with DENV2. Then, bioinformatics analysis was used to identify significant differentially expressed genes and the associated biological processes. Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was performed to verify the sequencing data. A total of 1239 DEGs were found by transcriptional analysis of C6/36 cells that were infected and uninfected with dengue virus, among which 1133 were upregulated and 106 were downregulated. Further bioinformatics analysis showed that the upregulated DEGs were significantly enriched in signaling pathways such as the MAPK, Hippo, FoxO, Wnt, mTOR, and Notch; metabolic pathways and cellular physiological processes such as autophagy, endocytosis, and apoptosis. Downregulated DEGs were mainly enriched in DNA replication, pyrimidine metabolism, and repair pathways, including BER, NER, and MMR. The qRT-PCR results showed that the concordance between the RNA-Seq and RT-qPCR data was very high (92.3%). The results of this study provide more information about DENV2 infection of C6/36 cells at the transcriptome level, laying a foundation for further research on mosquito vector-virus interactions. These data provide candidate antiviral genes that can be used for further functional verification in the future.
登革病毒(DENV)是黄病毒科的一个属成员,可引起登革热(DF)和更严重的疾病,因此在全球造成了沉重负担。作为 DENV 的主要媒介,蚊子是一个严重的危害。感染后,它们会诱导出复杂的宿主-病原体相互作用机制。我们的目标是在同源、敏感和可重复的 C6/36 细胞载体中进一步研究病毒的相互作用机制。转录组测序(RNA-Seq)技术被应用于感染 DENV2 的 C6/36 细胞的宿主转录谱。然后,生物信息学分析用于识别显著差异表达基因和相关的生物过程。定量逆转录聚合酶链反应(qRT-PCR)用于验证测序数据。通过对感染和未感染登革病毒的 C6/36 细胞进行转录分析,共发现 1239 个差异表达基因,其中 1133 个上调,106 个下调。进一步的生物信息学分析表明,上调的差异表达基因在 MAPK、Hippo、FoxO、Wnt、mTOR 和 Notch 等信号通路以及自噬、内吞和凋亡等代谢途径和细胞生理过程中显著富集。下调的差异表达基因主要富集在 DNA 复制、嘧啶代谢和修复途径,包括 BER、NER 和 MMR。qRT-PCR 结果表明,RNA-Seq 和 RT-qPCR 数据之间的一致性非常高(92.3%)。本研究结果为 DENV2 感染 C6/36 细胞在转录组水平上提供了更多信息,为进一步研究蚊媒-病毒相互作用奠定了基础。这些数据为今后进一步的功能验证提供了候选抗病毒基因。