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长链非编码RNA分析:高致病性新城疫病毒感染鸡胚内脏组织中的严重致病性——与无毒力疫苗病毒的比较

Long Non-Coding RNA Analysis: Severe Pathogenicity in Chicken Embryonic Visceral Tissues Infected with Highly Virulent Newcastle Disease Virus-A Comparison to the Avirulent Vaccine Virus.

作者信息

Sha Yuxin, Liu Xinxin, Yan Weiwen, Wang Mengjun, Li Hongjin, Jiang Shanshan, Wang Sijie, Ren Yongning, Zhang Kexin, Yin Renfu

机构信息

State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Key Laboratory of Zoonosis Research, Ministry of Education, Department of Preventive Veterinary Medicine, College of Veterinary Medicine, Jilin University, Changchun 130062, China.

College of Food Science and Engineering, Jilin University, Changchun 130062, China.

出版信息

Microorganisms. 2024 May 11;12(5):971. doi: 10.3390/microorganisms12050971.

DOI:10.3390/microorganisms12050971
PMID:38792800
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11123907/
Abstract

There are significant variations in pathogenicity among different virulent strains of the Newcastle disease virus (NDV). Virulent NDV typically induces severe pathological changes and high mortality rates in infected birds, while avirulent NDV usually results in asymptomatic infection. Currently, the understanding of the specific mechanisms underlying the differences in host pathological responses and symptoms caused by various virulent NDV strains remains limited. Long non-coding RNA (lncRNA) can participate in a range of biological processes and plays a crucial role in viral infection and replication. Therefore, this study employed RNA-Seq to investigate the transcriptional profiles of chicken embryos' visceral tissues (CEVTs) infected with either the virulent NA-1 strain or avirulent LaSota strain at 24 hpi and 36 hpi. Using bioinformatic methods, we obtained a total of 2532 lncRNAs, of which there were 52 and 85 differentially expressed lncRNAs at 24 hpi and 36 hpi, respectively. LncRNA analysis revealed that the severe pathological changes and symptoms induced by virulent NDV infection may be partially attributed to related target genes, regulated by differentially expressed lncRNAs such as MSTRG.1545.5, MSTRG.14601.6, MSTRG.7150.1, and MSTRG.4481.1. Taken together, these findings suggest that virulent NDV infection exploits the host's metabolic resources and exerts an influence on the host's metabolic processes, accompanied by excessive activation of the immune response. This impacts the growth and development of each system of CEVTs, breaches the blood-brain barrier, inflicts severe damage on the nervous system, and induces significant lesions. These observations may be attributed to variations in pathology. Consequently, novel insights were obtained into the intricate regulatory mechanisms governing NDV and host interactions. This will aid in unraveling the molecular mechanisms underlying both virulent and avirulent forms of NDV infection.

摘要

新城疫病毒(NDV)不同毒株的致病性存在显著差异。强毒株NDV通常会在感染禽类中引发严重的病理变化和高死亡率,而弱毒株NDV通常导致无症状感染。目前,对于不同强毒株NDV引起宿主病理反应和症状差异的具体机制了解仍然有限。长链非编码RNA(lncRNA)可参与一系列生物学过程,在病毒感染和复制中发挥关键作用。因此,本研究采用RNA测序技术,调查在感染后24小时和36小时感染强毒株NA-1或弱毒株LaSota的鸡胚内脏组织(CEVTs)的转录谱。通过生物信息学方法,我们共获得2532条lncRNA,其中在24小时和36小时分别有52条和85条差异表达的lncRNA。lncRNA分析表明,强毒株NDV感染诱导的严重病理变化和症状可能部分归因于相关靶基因,这些靶基因受MSTRG.1545.5、MSTRG.14601.6、MSTRG.7150.1和MSTRG.4481.1等差异表达lncRNA的调控。综上所述,这些发现表明,强毒株NDV感染利用宿主的代谢资源并对宿主的代谢过程产生影响,同时伴随着免疫反应的过度激活。这影响了CEVTs各系统生长发育,破坏血脑屏障,对神经系统造成严重损害并引发显著病变。这些观察结果可能归因于病理学差异。因此,获得了关于NDV与宿主相互作用复杂调控机制的新见解。这将有助于阐明强毒株和弱毒株NDV感染的分子机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d55/11123907/fd5891fd2da1/microorganisms-12-00971-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d55/11123907/61f4539dfd01/microorganisms-12-00971-g001a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d55/11123907/38191f7343ec/microorganisms-12-00971-g002a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d55/11123907/f1c9ea01ea9c/microorganisms-12-00971-g003a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d55/11123907/4e5d1040d0c5/microorganisms-12-00971-g004a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d55/11123907/8dc67eaeba54/microorganisms-12-00971-g005a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d55/11123907/fd5891fd2da1/microorganisms-12-00971-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d55/11123907/61f4539dfd01/microorganisms-12-00971-g001a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d55/11123907/38191f7343ec/microorganisms-12-00971-g002a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d55/11123907/f1c9ea01ea9c/microorganisms-12-00971-g003a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d55/11123907/4e5d1040d0c5/microorganisms-12-00971-g004a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d55/11123907/8dc67eaeba54/microorganisms-12-00971-g005a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d55/11123907/fd5891fd2da1/microorganisms-12-00971-g006.jpg

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SLC1A3 facilitates Newcastle disease virus replication by regulating glutamine catabolism.
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