African Swine Fever Virus pI215L Negatively Regulates cGAS-STING Signaling Pathway through Recruiting RNF138 to Inhibit K63-Linked Ubiquitination of TBK1

生物 泛素 病毒学 坦克结合激酶1 病毒 信号转导 基因 丝裂原活化蛋白激酶激酶 遗传学 细胞生物学 工程类 航空航天工程 蛋白激酶C
作者
Li Huang,Wenjie Xu,Hongyang Liu,Mengdi Xue,Xiaohong Liu,Kunli Zhang,Liang Hu,Jiangnan Li,Xuemin Liu,Zhida Xiang,Jun Zheng,Changyao Li,Weiye Chen,Zhigao Bu,Tao Xiong,Changjiang Weng
出处
期刊:Journal of Immunology [American Association of Immunologists]
卷期号:207 (11): 2754-2769 被引量:77
标识
DOI:10.4049/jimmunol.2100320
摘要

Abstract African swine fever is a severe animal infectious disease caused by African swine fever virus (ASFV), and the morbidity and mortality associated with virulent ASFV isolates are as high as 100%. Previous studies showed that the ability of ASFV to antagonize IFN production is closely related to its pathogenicity. Here, we report that ASFV HLJ/18 infection induced low levels of type I IFN and inhibited cGMP-AMP–induced type I IFN production in porcine alveolar macrophages that were isolated from specific pathogen-free Landrace piglets. Subsequently, an unbiased screen was performed to screen the ASFV genes with inhibitory effects on the type I IFN production. ASFV pI215L, a viral E2 ubiquitin–conjugating enzyme, was identified as one of the strongest inhibitory effectors on the production of type I IFN. Knockdown of pI215L expression inhibited ASFV replication and enhanced IFN-β production. However, inhibition of type I IFN production by pI215L was independent of its E2 enzyme activity. Furthermore, we found that pI215L inhibited type I IFN production and K63-linked polyubiquitination of TANK-binding kinase 1 through pI215L-binding RING finger protein 138 (RNF138). ASFV pI215L enhanced the interaction between RNF138 and RNF128 and promoted RNF138 to degrade RNF128, which resulted in reduced K63-linked polyubiquitination of TANK-binding kinase 1 and type І IFN production. Taken together, our findings reveal a novel immune escape mechanism of ASFV, which provides a clue to the design and development of an immune-sensitive attenuated live vaccine.
最长约 10秒,即可获得该文献文件

科研通智能强力驱动
Strongly Powered by AbleSci AI
更新
PDF的下载单位、IP信息已删除 (2025-6-4)

科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
骆烙完成签到 ,获得积分20
1秒前
2秒前
朴子完成签到 ,获得积分10
3秒前
3秒前
韩嘉琦发布了新的文献求助10
5秒前
所所应助xjl采纳,获得10
6秒前
完美世界应助黄启迪采纳,获得10
7秒前
zhangsir发布了新的文献求助10
8秒前
久别完成签到,获得积分10
9秒前
10秒前
12秒前
慕青应助正直如松采纳,获得10
13秒前
陶醉的念之完成签到,获得积分10
13秒前
书记完成签到,获得积分10
15秒前
风趣的语蕊完成签到,获得积分10
20秒前
可爱的函函应助书记采纳,获得10
20秒前
21秒前
星辰大海应助韩嘉琦采纳,获得10
22秒前
2哇哇哇完成签到,获得积分10
23秒前
浪麻麻完成签到 ,获得积分10
24秒前
正直如松发布了新的文献求助10
27秒前
30秒前
仁爱的寻凝完成签到,获得积分10
30秒前
香蕉觅云应助zhaxiao采纳,获得10
30秒前
希望天下0贩的0应助zhaxiao采纳,获得10
30秒前
Gauss应助zhaxiao采纳,获得30
30秒前
Gauss应助zhaxiao采纳,获得30
30秒前
大宝君应助zhaxiao采纳,获得30
30秒前
隐形曼青应助zhaxiao采纳,获得10
30秒前
Flipped完成签到,获得积分10
32秒前
33秒前
Akim应助土匪猫采纳,获得10
34秒前
顺顺完成签到,获得积分10
34秒前
35秒前
CodeCraft应助tao采纳,获得10
35秒前
陈煜完成签到 ,获得积分10
37秒前
Neshama完成签到,获得积分10
38秒前
虚幻靖易完成签到,获得积分10
41秒前
41秒前
42秒前
高分求助中
【重要!!请各位用户详细阅读此贴】科研通的精品贴汇总(请勿应助) 10000
Plutonium Handbook 1000
Three plays : drama 1000
International Code of Nomenclature for algae, fungi, and plants (Madrid Code) (Regnum Vegetabile) 1000
Semantics for Latin: An Introduction 999
Psychology Applied to Teaching 14th Edition 600
Robot-supported joining of reinforcement textiles with one-sided sewing heads 580
热门求助领域 (近24小时)
化学 材料科学 医学 生物 工程类 有机化学 生物化学 物理 内科学 纳米技术 计算机科学 化学工程 复合材料 遗传学 基因 物理化学 催化作用 冶金 细胞生物学 免疫学
热门帖子
关注 科研通微信公众号,转发送积分 4088500
求助须知:如何正确求助?哪些是违规求助? 3627287
关于积分的说明 11501263
捐赠科研通 3340128
什么是DOI,文献DOI怎么找? 1836165
邀请新用户注册赠送积分活动 904264
科研通“疑难数据库(出版商)”最低求助积分说明 822174