Manganese and the cGAS-STING Pathway in Infectious Mononucleosis Caused by Epstein-Barr Virus Infection

Viral Immunol. 2023 Jan;36(1):48-54. doi: 10.1089/vim.2022.0108. Epub 2022 Dec 9.

Abstract

To study the clinical significance of manganese (Mn) in the serum of children with infectious mononucleosis (IM) caused by Epstein-Barr virus (EBV) infection, we analyzed the correlation between Mn and the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway and explored the immune pathogenesis of EBV infection. Children diagnosed with IM comprised the IM group, and healthy children during the same period were selected as the normal control group. Real-time reverse transcription-polymerase chain reaction was used to detect the mRNA expression levels of cGAS, STING, Tank-binding kinase 1 (TBK1), interferon regulatory factor 3 (IRF3), and related inflammatory factors, and Mn in serum was detected by inductively coupled plasma mass spectrometry. Interferon (IFN)-α and IFN-β expression levels in serum were detected by enzyme-linked immunosorbent assay, and the correlation between Mn levels and clinical manifestations and laboratory tests was analyzed. Mn levels and the expression levels of cGAS, STING, and related inflammatory factors were significantly higher in children with IM than in healthy children. Furthermore, Mn levels in children with IM were positively correlated with the expression levels of cGAS and related inflammatory factors. Thus, Mn, cGAS, STING, and inflammatory cytokines may be involved in the immune mechanism of IM caused by EBV infection.

Keywords: Epstein-Barr virus; Mn; cGAS–STING signaling pathway; immune response; infectious mononucleosis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Child
  • Epstein-Barr Virus Infections*
  • Herpesvirus 4, Human
  • Humans
  • Infectious Mononucleosis*
  • Interferons
  • Manganese
  • Nucleotidyltransferases / genetics
  • Nucleotidyltransferases / metabolism

Substances

  • Manganese
  • Nucleotidyltransferases
  • Interferons