FAT10 Is Critical in Influenza A Virus Replication by Inhibiting Type I IFN
The H5N1 avian influenza virus causes severe disease and high mortality, making it a major public health concern worldwide. The virus uses the host cellular machinery for several steps of its life cycle. In this report, we observed overexpression of the ubiquitin-like protein FAT10 following live H5...
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| Published in | The Journal of immunology (1950) Vol. 197; no. 3; pp. 824 - 833 |
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| Main Authors | , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
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United States
01.08.2016
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| Abstract | The H5N1 avian influenza virus causes severe disease and high mortality, making it a major public health concern worldwide. The virus uses the host cellular machinery for several steps of its life cycle. In this report, we observed overexpression of the ubiquitin-like protein FAT10 following live H5N1 virus infection in BALB/c mice and in the human respiratory epithelial cell lines A549 and BEAS-2B. Further experiments demonstrated that FAT10 increased H5N1 virus replication and decreased the viability of infected cells. Total RNA extracted from H5N1 virus–infected cells, but not other H5N1 viral components, upregulated FAT10, and this process was mediated by the retinoic acid–induced protein I-NF-κB signaling pathway. FAT10 knockdown in A549 cells upregulated type I IFN mRNA expression and enhanced STAT1 phosphorylation during live H5N1 virus infection. Taken together, our data suggest that FAT10 was upregulated via retinoic acid–induced protein I and NF-κB during H5N1 avian influenza virus infection. And the upregulated FAT10 promoted H5N1 viral replication by inhibiting type I IFN. |
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| AbstractList | The H5N1 avian influenza virus causes severe disease and high mortality, making it a major public health concern worldwide. The virus uses the host cellular machinery for several steps of its life cycle. In this report, we observed overexpression of the ubiquitin-like protein FAT10 following live H5N1 virus infection in BALB/c mice and in the human respiratory epithelial cell lines A549 and BEAS-2B. Further experiments demonstrated that FAT10 increased H5N1 virus replication and decreased the viability of infected cells. Total RNA extracted from H5N1 virus–infected cells, but not other H5N1 viral components, upregulated FAT10, and this process was mediated by the retinoic acid–induced protein I-NF-κB signaling pathway. FAT10 knockdown in A549 cells upregulated type I IFN mRNA expression and enhanced STAT1 phosphorylation during live H5N1 virus infection. Taken together, our data suggest that FAT10 was upregulated via retinoic acid–induced protein I and NF-κB during H5N1 avian influenza virus infection. And the upregulated FAT10 promoted H5N1 viral replication by inhibiting type I IFN. The H5N1 avian influenza virus causes severe disease and high mortality, making it a major public health concern worldwide. The virus uses the host cellular machinery for several steps of its life cycle. In this report, we observed overexpression of the ubiquitin-like protein FAT10 following live H5N1 virus infection in BALB/c mice and in the human respiratory epithelial cell lines A549 and BEAS-2B. Further experiments demonstrated that FAT10 increased H5N1 virus replication and decreased the viability of infected cells. Total RNA extracted from H5N1 virus-infected cells, but not other H5N1 viral components, upregulated FAT10, and this process was mediated by the retinoic acid-induced protein I-NF- Kappa B signaling pathway. FAT10 knockdown in A549 cells upregulated type I IFN mRNA expression and enhanced STAT1 phosphorylation during live H5N1 virus infection. Taken together, our data suggest that FAT10 was upregulated via retinoic acid-induced protein I and NF- Kappa B during H5N1 avian influenza virus infection. And the upregulated FAT10 promoted H5N1 viral replication by inhibiting type I IFN. |
| Author | Zhang, Qingchao Li, Ning Xie, Peng Liu, Song Sun, Yang Liu, Qiang Lu, Huijun Li, Shunwang Zhang, Yanli Zhang, Yanxu Deng, Jiejie Jin, Ningyi Zhou, Huandi Zhang, Michael Q Li, Xiao Tian, Mingyao Jiang, Chengyu Tang, Jun Zhao, Yan Yang, Ning |
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| SubjectTerms | Animals Avian influenza virus Blotting, Western Cell Line Gene Knockdown Techniques Humans Influenza A virus Influenza A Virus, H5N1 Subtype Interferon Type I - biosynthesis Mice Mice, Inbred BALB C Oligonucleotide Array Sequence Analysis Orthomyxoviridae Infections - immunology Orthomyxoviridae Infections - metabolism Polymerase Chain Reaction Respiratory Mucosa - immunology Respiratory Mucosa - metabolism Respiratory Mucosa - virology Ubiquitins - metabolism Up-Regulation Virus Replication - physiology |
| Title | FAT10 Is Critical in Influenza A Virus Replication by Inhibiting Type I IFN |
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