Nonstructural protein (NS1) of human parvovirus B19 stimulates host innate immunity and blunts the exogenous type I interferon signaling in vitro.
B19 virus is a non-enveloped DNA virus and belongs to the family of parvoviridae. There are two large open reading frames (ORFs), nonstructural protein (NS1) and two capsid proteins (VP1 and VP2). Host innate immune responses form the first line of defense against many pathogen invasion. How B19 virus, especially its encoded viral proteins interacts with host innate immune system remains unknown. In this study we aim to investigate the effect of NS1 on the host innate immune response and exogenous type I IFN signaling. Here we found that the type I IFN can be stimulated by NS1. Interestingly, NS1 also plays an important role in inhibiting the exogenous type I IFN signaling at p-STAT1, ISRE and ISGs levels. We concluded that NS1 may play pivotal role in evading the host immune surveillance. Our data shed novel light on the pathogenesis of B19 viral infection and virus evasion strategies.
Institute of Blood Transfusion, Chinese Academy of Medical Sciences and Peking Union Medical College, Chengdu, Sichuan 610052, China; Provincial Key Laboratory for Transfusion-transmitted Diseases of Sichuan Province, Chengdu 610052, China.
Jianqin
J
Wu
Institute of Blood Transfusion, Chinese Academy of Medical Sciences and Peking Union Medical College, Chengdu, Sichuan 610052, China; Provincial Key Laboratory for Transfusion-transmitted Diseases of Sichuan Province, Chengdu 610052, China.
Xu
X
Chen
Institute of Blood Transfusion, Chinese Academy of Medical Sciences and Peking Union Medical College, Chengdu, Sichuan 610052, China; Provincial Key Laboratory for Transfusion-transmitted Diseases of Sichuan Province, Chengdu 610052, China.
Haiyan
H
Ye
Institute of Blood Transfusion, Chinese Academy of Medical Sciences and Peking Union Medical College, Chengdu, Sichuan 610052, China; Provincial Key Laboratory for Transfusion-transmitted Diseases of Sichuan Province, Chengdu 610052, China.
Min
M
Yao
Institute of Blood Transfusion, Chinese Academy of Medical Sciences and Peking Union Medical College, Chengdu, Sichuan 610052, China; Provincial Key Laboratory for Transfusion-transmitted Diseases of Sichuan Province, Chengdu 610052, China.
Shilin
S
Li
Institute of Blood Transfusion, Chinese Academy of Medical Sciences and Peking Union Medical College, Chengdu, Sichuan 610052, China; Provincial Key Laboratory for Transfusion-transmitted Diseases of Sichuan Province, Chengdu 610052, China; Toronto General Research Institute, University Health Network, University of Toronto, Toronto, Ontario M5 G 1L6, Canada. Electronic address: limin_chen_99@yahoo.com.
Limin
L
Chen
D003001:Cloning, Molecular; D015870:Gene Expression; D016679:Genome, Viral; D006367:HeLa Cells; D054884:Host-Pathogen Interactions / Q000276:immunology*; D006801:Humans; D007113:Immunity, Innate; D007370:Interferon Type I / Q000378:metabolism*; D010322:Parvoviridae Infections / Q000276:immunology* / Q000378:metabolism* / Q000821:virology; D016732:Parvovirus B19, Human / Q000235:genetics / Q000276:immunology*; D010766:Phosphorylation; D050794:STAT1 Transcription Factor / Q000378:metabolism; D015398:Signal Transduction; D017361:Viral Nonstructural Proteins / Q000235:genetics / Q000276:immunology*
D007370:Interferon Type I; C106202:NS1 protein, parvovirus; D050794:STAT1 Transcription Factor; D017361:Viral Nonstructural Proteins
B19 virus; NS1; Type I IFN signaling