Demethylation around the transcriptional start site of the IFN-β gene induces IFN-β production and protection against influenza virus infection

• Published in: Biochemical and biophysical research communications Vol. 520; no. 2; pp. 269 - 276
• Main Authors: Nishioka, Keisuke, Daidoji, Tomo, Nakaya, Takaaki
• Format: Journal Article
• Language: English
• Published: Elsevier Inc 03.12.2019
• Subjects: CpG methylation; Epigenetics; IFN-Beta; Influenza virus; Viral infection; Epigenetics; IFN-Beta; CpG methylation; Influenza virus; Viral infection
• ISSN: 0006-291X; 1090-2104
• DOI: 10.1016/j.bbrc.2019.09.136

Seasonal influenza is related to lifestyle-associated risk factors and it has been suggested that the epigenetic state of the individual plays an important role in the severity of infection. It is well known that epigenetics stringently regulate gene expression in each tissue and that aberrant epigenetic states can influence disease development. Despite some studies, limited information is available on changes in epigenetic states before and after influenza virus infection; in particular, it is unknown whether the epigenetic state at specific sites affects subsequent infection. Here, we analyzed CpG methylation states in clones derived from human primary small airway epithelial cells with the same genetic background but different viral replication rates. Our study revealed that demethylating CpGs downstream of the IFN-β transcription start site using a CRISPR/dCas9 system suppressed viral replication during subsequent influenza virus infection. Thus, our observations suggest that epigenome editing might provide adequate protection against the influenza virus. •Epigenetic state is related to influenza infection.•We analyzed CpG methylation state among human cells with the same genetic background.•Demethylation at CpGs downstream of IFN-β start codon suppressed viral replication.•Epigenome editing might be protective against influenza virus.