Transcriptome-wide 5-methylcytosine modification profiling of long non-coding RNAs in A549 cells infected with H1N1 influenza A virus

BACKGROUND: In recent years, accumulating evidences have revealed that influenza A virus (IAV) infections induce significant differential expression of host long noncoding RNAs (lncRNAs), some of which play important roles in the regulation of virus-host interactions and determining the virus pathogenesis.

However, whether these lncRNAs bear post-translational modifications and how their differential expression is regulated remain largely unknown.

In this study, the transcriptome-wide 5-methylcytosine (m(5)C) modification of lncRNAs in A549 cells infected with an H1N1 influenza A virus was analyzed and compared with uninfected cells by Methylated RNA immunoprecipitation sequencing (MeRIP-Seq).

RESULTS: Our data identified 1317 upregulated m(5)C peaks and 1667 downregulated peaks in the H1N1 infected group.

Gene ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses showed that the differentially modified lncRNAs were associated with protein modification, organelle localization, nuclear export and other biological processes.

Furthermore, conjoint analysis of the differentially modified (DM) and differentially expressed (DE) lncRNAs identified 143 ‘hyper-up’, 81 ‘hypo-up’, 6 ‘hypo-down’ and 4 ‘hyper-down’ lncRNAs.

GO and KEGG analyses revealed that these DM and DE lncRNAs were predominantly associated with pathogen recognition and disease pathogenesis pathways, indicating that m(5)C modifications could play an important role in the regulation of host response to IAV replication by modulating the expression and/or stability of lncRNAs.

CONCLUSION: This study presented the first m(5)C modification profile of lncRNAs in A549 cells infected with IAV and demonstrated a significant alteration of m(5)C modifications on host lncRNAs upon IAV infection.

These data could give a reference to future researches on the roles of m(5)C methylation in virus infection.

SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12864-023-09432-z.