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伪狂犬病病毒利用N-甲基腺苷修饰来促进病毒复制。

Pseudorabies virus exploits N-methyladenosine modification to promote viral replication.

作者信息

Yu Pei-Lun, Wu Rui, Cao San-Jie, Wen Yi-Ping, Huang Xiao-Bo, Zhao Shan, Lang Yi-Fei, Zhao Qin, Lin Ju-Chun, Du Sen-Yan, Yu Shu-Min, Yan Qi-Gui

机构信息

Department of Preventive Veterinary Medicine, Swine Disease Research Center, College of Veterinary Medicine, Sichuan Agricultural University, Chengdu, China.

Key Laboratory of Animal Disease and Human Health of Sichuan Province, Sichuan Agricultural University, Chengdu, China.

出版信息

Front Microbiol. 2023 Feb 3;14:1087484. doi: 10.3389/fmicb.2023.1087484. eCollection 2023.

DOI:10.3389/fmicb.2023.1087484
PMID:36819040
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9936159/
Abstract

INTRODUCTION

Pseudorabies virus (PRV) is the pathogenic virus of porcine pseudorabies (PR), belonging to the family. PRV has a wide range of hosts and in recent years has also been reported to infect humans. N-methyladenosine (mA) modification is the major pathway of RNA post-transcriptional modification. Whether mA modification participates in the regulation of PRV replication is unknown.

METHODS

Here, we investigated that the mA modification was abundant in the PRV transcripts and PRV infection affected the epitranscriptome of host cells. Knockdown of cellular mA methyltransferases METTL3 and METTL14 and the specific binding proteins YTHDF2 and YTHDF3 inhibited PRV replication, while silencing of demethylase ALKBH5 promoted PRV output. The overexpression of METTL14 induced more efficient virus proliferation in PRV-infected PK15 cells. Inhibition of mA modification by 3-deazaadenosine (3-DAA), a mA modification inhibitor, could significantly reduce viral replication.

RESULTS AND DISCUSSION

Taken together, mA modification played a positive role in the regulation of PRV replication and gene expression. Our research revealed mA modification sites in PRV transcripts and determined that mA modification dynamically mediated the interaction between PRV and host.

摘要

引言

伪狂犬病病毒（PRV）是猪伪狂犬病（PR）的致病病毒，属于 科。PRV宿主范围广泛，近年来也有报道称其可感染人类。N-甲基腺苷（mA）修饰是RNA转录后修饰的主要途径。mA修饰是否参与PRV复制的调控尚不清楚。

方法

在此，我们研究发现PRV转录本中存在丰富的mA修饰，且PRV感染会影响宿主细胞的表观转录组。敲低细胞内的mA甲基转移酶METTL3和METTL14以及特异性结合蛋白YTHDF2和YTHDF3可抑制PRV复制，而沉默去甲基酶ALKBH5则促进PRV产生。在PRV感染的PK15细胞中过表达METTL14可诱导更高效的病毒增殖。用mA修饰抑制剂3-脱氮腺苷（3-DAA）抑制mA修饰可显著降低病毒复制。

结果与讨论

综上所述，mA修饰在PRV复制和基因表达的调控中发挥了积极作用。我们的研究揭示了PRV转录本中的mA修饰位点，并确定mA修饰动态介导了PRV与宿主之间的相互作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d4b6/9936159/1c9809503e5d/fmicb-14-1087484-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d4b6/9936159/ac7381d4a134/fmicb-14-1087484-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d4b6/9936159/6ab4e8ea031c/fmicb-14-1087484-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d4b6/9936159/5ad76721b8ad/fmicb-14-1087484-g003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d4b6/9936159/bec55300af16/fmicb-14-1087484-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d4b6/9936159/f3bd2c47d730/fmicb-14-1087484-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d4b6/9936159/d7d77cc52754/fmicb-14-1087484-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d4b6/9936159/eb2be595e877/fmicb-14-1087484-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d4b6/9936159/1c9809503e5d/fmicb-14-1087484-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d4b6/9936159/ac7381d4a134/fmicb-14-1087484-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d4b6/9936159/6ab4e8ea031c/fmicb-14-1087484-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d4b6/9936159/5ad76721b8ad/fmicb-14-1087484-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d4b6/9936159/75876923a9b6/fmicb-14-1087484-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d4b6/9936159/bec55300af16/fmicb-14-1087484-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d4b6/9936159/f3bd2c47d730/fmicb-14-1087484-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d4b6/9936159/d7d77cc52754/fmicb-14-1087484-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d4b6/9936159/eb2be595e877/fmicb-14-1087484-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d4b6/9936159/1c9809503e5d/fmicb-14-1087484-g009.jpg

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