Department of Infectious Diseases, College of Veterinary Medicine, University of Georgia, Athens, Georgia, United States of America.
PLoS One. 2023 Nov 14;18(11):e0294173. doi: 10.1371/journal.pone.0294173. eCollection 2023.
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.
副粘病毒是负义、单链 RNA 病毒，与人类和动物的许多疾病有关。1972 年，在澳大利亚，从患有肺出血病变濒死的小鼠（Mus musculus）中首次分离到 J 副粘病毒（JPV）。2016 年，JPV 被分类到新建立的杰利翁病毒属。在世界范围内的野生动物种群中，新型杰利翁病毒正在被发现。然而，杰利翁病毒感染对宿主基因表达的影响仍未被描述。为了解决这个问题，在感染 JPV 的小鼠成纤维细胞中收集了在感染后 2、4、8、12、16、24 和 48 小时（hpi）的细胞 RNA，并在 Illumina NextSeq 平台上使用单端 75 个碱基（SE75）测序化学法进行测序。使用 Tophat2-Cufflinks-Cuffdiff 协议，在每个时间点识别病毒感染的重复样本和对照重复样本之间的差异表达基因（DEG）。在 2 hpi 时，在 JPV 感染的细胞中鉴定到 11 个 DEG，而在 48 hpi 时检测到 1837 个 DEG。GO 分析确定，早期时间点的基因参与干扰素反应，而在后期时间点，基因则转向参与抗原加工和呈递过程。在 48 hpi 时，KEGG 分析表明，检测到的许多 DEG 都参与了对免疫反应很重要的途径。qRT-PCR 验证了在 JPV 感染过程中，Rtp4、Ifit3、Mx2 和 Stat2 均上调，而 G0s2 下调。在 JPV 感染后，小鼠成纤维细胞中炎症和抗病毒因子的表达发生显著变化。本研究为杰利翁病毒感染中宿主免疫的不同分支提供了重要的见解。了解杰利翁病毒的致病机制将为预防和控制可能由该病毒组引起的潜在疾病提供更好的策略。
