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Long noncoding RNA EGOT negatively affects the antiviral response and favors HCV replication
Author(s) -
Carnero Elena,
Barriocanal Marina,
Prior Celia,
Pablo Unfried Juan,
Segura Victor,
Guruceaga Elizabeth,
Enguita Mónica,
Smerdou Cristian,
Gastaminza Pablo,
Fortes Puri
Publication year - 2016
Publication title -
embo reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.584
H-Index - 184
eISSN - 1469-3178
pISSN - 1469-221X
DOI - 10.15252/embr.201541763
Subject(s) - biology , semliki forest virus , rna , virology , viral replication , long non coding rna , hepatitis c virus , interferon , transcriptome , rna virus , virus , downregulation and upregulation , gene expression , gene , genetics
Abstract The role of long noncoding RNA s (lnc RNA s) in viral infection is poorly studied. We have identified hepatitis C virus ( HCV )‐ S timulated lnc R NA s ( CSR s) by transcriptome analysis. Interestingly, two of these CSR s ( PVT 1 and UCA 1) play relevant roles in tumorigenesis, providing a novel link between HCV infection and development of liver tumors. Expression of some CSR s seems induced directly by HCV , while others are upregulated by the antiviral response against the virus. In fact, activation of pathogen sensors induces the expression of CSR 32/ EGOT . RIG ‐I and the RNA ‐activated kinase PKR sense HCV RNA , activate NF ‐κB and upregulate EGOT . EGOT is increased in the liver of patients infected with HCV and after infection with influenza or Semliki Forest virus ( SFV ). Genome‐wide guilt‐by‐association studies predict that EGOT may function as a negative regulator of the antiviral pathway. Accordingly, EGOT depletion increases the expression of several interferon‐stimulated genes and leads to decreased replication of HCV and SFV . Our results suggest that EGOT is a lnc RNA induced after infection that increases viral replication by antagonizing the antiviral response.