1. MOV10 sequesters the RNP of influenza A virus in the cytoplasm and is antagonized by viral NS1 protein
- Author
-
Shan Cen, Jianwei Wang, Zichen Xiong, Di Zhang, Hong Sun, Siqi Hu, Xiaoman Liu, Shan Mei, Chen Liang, Jian Li, Fei Guo, Fengwen Xu, Fei Zhao, Xiaoxiao Zhao, and Lijuan Yin
- Subjects
Cytoplasm ,viruses ,Hepatitis C virus ,Biology ,Viral Nonstructural Proteins ,medicine.disease_cause ,Biochemistry ,03 medical and health sciences ,P-bodies ,Influenza A virus ,medicine ,Humans ,Molecular Biology ,030304 developmental biology ,0303 health sciences ,Host (biology) ,030302 biochemistry & molecular biology ,Cell Biology ,biology.organism_classification ,Virology ,Nucleoprotein ,HEK293 Cells ,Ribonucleoproteins ,Vesicular stomatitis virus ,A549 Cells ,Proteolysis ,Intracisternal A-Particle ,Lysosomes ,RNA Helicases - Abstract
MOV10 has emerged as an important host antiviral factor. MOV10 not only inhibits various viruses, including human immunodeficiency virus type 1, hepatitis C virus and vesicular stomatitis virus, but also restricts the activity of retroelements long interspersed nucleotide element-1, Alu, SVA and intracisternal A particles. Here, we report that MOV10 suppresses influenza A virus infection through interacting with viral nucleoprotein (NP), sequestering viral RNP in the cytoplasm and causing the degradation of viral vRNA. The antiviral activity of MOV10 depends on the integrity of P-bodies. We also found that the antiviral activity of MOV10 is partially countered by viral NS1 protein that interferes with the interaction of MOV10 with viral NP and causes MOV10 degradation through the lysosomal pathway. Moreover, NS1-defective influenza A virus is more susceptible to MOV10 restriction. Our data not only expand the antiviral spectrum of MOV10 but also reveal the NS1 protein as the first viral antagonist of MOV10.
- Published
- 2018