4.7 Article

Long noncoding RNA IRF1-AS is associated with peste des petits ruminants infection

Journal

VETERINARY RESEARCH
Volume 53, Issue 1, Pages -

Publisher

BMC
DOI: 10.1186/s13567-022-01105-1

Keywords

PPRV; lncRNAs; innate immune response; IRF1; IRF3

Funding

  1. National Natural Science, Foundation of China [32072895]
  2. National Key Research and Development Program of China [2021YFD1800500]

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This study demonstrates that PPRV infection can induce an innate immune response in caprine endometrial epithelial cells and identifies differentially expressed lncRNAs associated with immune response. The study also highlights the role of IRF1-AS in regulating the innate immune response and suggests it as a potential target for antiviral therapies against PPRV infection.
Peste des petits ruminants (PPR) is an acute and highly contagious disease and has long been a significant threat to small ruminant productivity worldwide. However, the molecular mechanism underlying host-PPRV interactions remains unclear and the long noncoding RNAs (lncRNAs) regulation of PPR virus (PPRV) infection has rarely been reported so far. Here, we first demonstrated that PPRV infection can induce an obvious innate immune response in caprine endometrial epithelial cells (EECs) at 48 h post-infection (hpi) with an MOI of 3. Subsequently, we determined that PPRV infection is associated with 191 significantly differentially expressed (SDE) lncRNAs, namely, 137 upregulated and 54 downregulated lncRNAs, in caprine EECs compared with mock control cells at 48 hpi by using deep sequencing technology. Importantly, bioinformatics preliminarily analyses revealed that these DE lncRNAs were closely related to the immune response. Furthermore, we identified a system of lncRNAs related to the immune response and focused on the role of lncRNA 10636385 (IRF1-AS) in regulating the innate immune response. Interestingly, we found that IRF1-AS was a potent positive regulator of IFN-beta and ISG production, which can significantly inhibit PPRV replication in host cells. In addition, our data revealed that IRF1-AS was positively correlated with its potential target gene, IRF1, which enhanced the activation of IRF3 and the expression of ISGs and interacted with IRF3. This study suggests that IRF1-AS could be a new host factor target for developing antiviral therapies against PPRV infection.

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