Evasion of Innate and Intrinsic Antiviral Pathways by the Zika Virus

Viruses

卷:11

TarynM. Serman¹  MichaelaU. Gack¹ 

[1] Department of Microbiology, The University of Chicago, Chicago, IL 60637, USA;

关键词: flavivirus;    zika virus;    innate immunity;    antiviral;    interferon;    stress response;    nonsense-mediated mrna decay;    autophagy;   

DOI  :  10.3390/v11100970

来源: DOAJ

【 摘 要 】

The Zika virus (ZIKV) is a recently emerged mosquito-borne flavivirus that, while typically asymptomatic, can cause neurological symptoms in adults and birth defects in babies born to infected mothers. The interactions of ZIKV with many different pathways in the human host ultimately determine successful virus replication and ZIKV-induced pathogenesis; however, the molecular mechanisms of such host-ZIKV interactions have just begun to be elucidated. Here, we summarize the recent advances that defined the mechanisms by which ZIKV antagonizes antiviral innate immune signaling pathways, with a particular focus on evasion of the type I interferon response in the human host. Furthermore, we describe emerging evidence that indicated the contribution of several cell-intrinsic mechanisms to an effective restriction of ZIKV infection, such as nonsense-mediated mRNA decay, stress granule formation, and “reticulophagy”, a type of selective autophagy. Finally, we summarize the recent work that identified strategies by which ZIKV modulated these intrinsic antiviral responses.

【 授权许可】

Unknown