Prototype foamy virus downregulates RelB expression to facilitate viral replication
Autor: | Juan Tan, Junshi Zhang, Xiaopeng Tuo, Chenchen Wang, Wentao Qiao, Yali Xu, Keli Chai |
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Rok vydání: | 2020 |
Předmět: |
0301 basic medicine
Small interfering RNA animal structures Transcription Genetic LTR Gene Expression RelB Virus Replication General Biochemistry Genetics and Molecular Biology Virus Cell Line 03 medical and health sciences Transactivation Viral Proteins 0302 clinical medicine Humans Promoter Regions Genetic lcsh:QH301-705.5 Research Articles Host factor biology RELB Transcription Factor RelB Terminal Repeat Sequences biology.organism_classification Virology Long terminal repeat 030104 developmental biology lcsh:Biology (General) Hepadnaviridae Viral replication 030220 oncology & carcinogenesis IP Spumavirus prototype foamy virus transcription Research Article |
Zdroj: | FEBS Open Bio FEBS Open Bio, Vol 10, Iss 10, Pp 2137-2148 (2020) |
ISSN: | 2211-5463 |
Popis: | Foamy viruses (FVs) establish lifelong latent infections without evident pathology in the host. The roles of cellular factors in FV replication are poorly understood. In this study, we demonstrate that RelB interacts with PFV Tas, and RelB decreases Tas‐dependent transactivation of PFV gene expression in turn. PFV infection downregulates the viral inhibitory host factor RelB, which otherwise restricts viral gene expression. Foamy viruses (FVs) are classified in the subfamily Spumaretrovirinae and bridge the gap between Orthoretrovirinae and Hepadnaviridae. FVs have strong cytopathic effects against cells cultured in vitro. However, they establish lifelong latent infections without evident pathology in the host. The roles of cellular factors in FV replication are poorly understood. To better understand this area, we determined the transcriptomes of HT1080 cells infected with prototype foamy virus (PFV) to measure the effect of PFV infection on the expression of cellular genes. We found that the level of RelB mRNA, a member of the nuclear factor‐κB (NF‐κB) protein family, was significantly decreased as a result of PFV infection, and this was further confirmed with real‐time PCR. Interestingly, overexpression of RelB reduced PFV replication, whereas its depletion using small interfering RNA increased PFV replication. This inhibitory effect of RelB results from diminished transactivation of the viral long terminal repeat (LTR) promoter and an internal promoter (IP) by viral Tas protein. Together, these data demonstrate that PFV infection downregulates the viral inhibitory host factor RelB, which otherwise restricts viral gene expression. |
Databáze: | OpenAIRE |
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