Regulation of host gene expression by J paramyxovirus.
Regulation of host gene expression by J paramyxovirus.
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DOI：
10.1371/journal.pone.0294173
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发表时间：
2023
期刊：
影响因子：
3.7
通讯作者：
中科院分区：
文献类型：
--
作者：
副粘病毒是与人类和动物中的许多疾病相关的负义单链RNA病毒。J副粘病毒（JPV）于1972年首次在澳大利亚从患有出血性肺损伤的濒死小鼠（Mus musculus）中分离出来。2016年，JPV被归类为新建立的Jeilong病毒属。在世界各地的野生动物种群中发现了新的吉隆病毒。然而，jeilongvirus感染对宿主基因表达的影响仍然没有得到表征。为了解决这个问题，在感染后2、4、8、12、16、24和48小时（hpi）收集来自JPV感染的小鼠成纤维细胞的细胞RNA，并在Illumina NextSeq平台上使用单端75个碱基对（SE 75）测序化学进行测序。使用Tophat 2-Cufflinks-Cuffdiff方案鉴定每个时间点病毒感染的重复和模拟重复之间的差异表达基因（DEG）。在2 hpi时，在JPV感染的细胞中鉴定出11个DEG，而在48 hpi时检测到1，837个DEG。GO分析确定，在较早的时间点的基因参与干扰素应答，而在较晚的时间点有向参与抗原加工和呈递过程的基因的转变。在48 hpi时，KEGG分析显示，检测到的许多DEG参与对免疫应答重要的途径。qRT-PCR证实在JPV感染过程中Rtp 4、Ifit 3、Mx2和Stat 2均上调，而G 0 s2下调。JPV感染后，小鼠成纤维细胞中炎性因子和抗病毒因子的表达发生显著变化。这项研究提供了重要的洞察宿主免疫的不同武器，介导的Jeilongvirus感染。了解Jeilong病毒的致病机制将导致更好的预防和控制可能由这组病毒引起的潜在疾病的策略。
Paramyxoviruses are negative-sense, single-stranded RNA viruses that are associated with numerous diseases in humans and animals. J paramyxovirus (JPV) was first isolated from moribund mice (Mus musculus) with hemorrhagic lung lesions in Australia in 1972. In 2016, JPV was classified into the newly established genus Jeilongvirus. Novel jeilongviruses are being discovered worldwide in wildlife populations. However, the effects of jeilongvirus infection on host gene expression remains uncharacterized. To address this, cellular RNA from JPV-infected mouse fibroblasts was collected at 2, 4, 8, 12, 16, 24, and 48 hours post-infection (hpi) and were sequenced using single-end 75 base pairs (SE75) sequencing chemistry on an Illumina NextSeq platform. Differentially expressed genes (DEGs) between the virus-infected replicates and mock replicates at each timepoint were identified using the Tophat2-Cufflinks-Cuffdiff protocol. At 2 hpi, 11 DEGs were identified in JPV-infected cells, while 1,837 DEGs were detected at 48 hpi. A GO analysis determined that the genes at the earlier timepoints were involved in interferon responses, while there was a shift towards genes that are involved in antigen processing and presentation processes at the later timepoints. At 48 hpi, a KEGG analysis revealed that many of the DEGs detected were involved in pathways that are important for immune responses. qRT-PCR verified that Rtp4, Ifit3, Mx2, and Stat2 were all upregulated during JPV infection, while G0s2 was downregulated. After JPV infection, the expression of inflammatory and antiviral factors in mouse fibroblasts changes significantly. This study provides crucial insight into the different arms of host immunity that mediate Jeilongvirus infection. Understanding the pathogenic mechanisms of Jeilongvirus will lead to better strategies for the prevention and control of potential diseases that may arise from this group of viruses.
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