MicroRNA let-7 Suppresses Influenza A Virus Infection by Targeting RPS16 and Enhancing Type I Interferon Response

Front Cell Infect Microbiol. 2022 Jul 7:12:904775. doi: 10.3389/fcimb.2022.904775. eCollection 2022.

Abstract

Given the frequent emergence of drug-resistant influenza virus strains and new highly pathogenic influenza virus strains, there is an urgent need to identify new antiviral drugs and targets. We found that influenza A virus (IAV) infection caused a significant decrease of microRNA let-7 expression in host cells; that overexpression of let-7 increased interferon expression and effectively inhibit IAV infection; and that let-7 targets the 3'-untranslated region (UTR) of the ribosomal protein 16 (RPS16) gene, decreasing its expression. Knocking down the expression of RPS16 increased the expression of type I interferon and inhibited viral replication. The present study uncovered the regulatory effect of let-7b and let-7f on influenza A infection, which is a potential biomarker of IAV infection. In addition, let-7 may be a promising therapeutic agent against influenza A.

Keywords: antivirals; influenza A virus; microRNA let-7; rps16; type I interferon.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antiviral Agents / pharmacology
  • Host-Pathogen Interactions
  • Humans
  • Influenza A virus
  • Influenza, Human* / drug therapy
  • Influenza, Human* / genetics
  • Interferon Type I* / metabolism
  • MicroRNAs* / genetics
  • Ribosomal Proteins / metabolism
  • Virus Replication

Substances

  • Antiviral Agents
  • Interferon Type I
  • MicroRNAs
  • Ribosomal Proteins
  • Rps16 protein, human
  • mirnlet7 microRNA, human