Measles Virus Matrix Protein Inhibits Host Cell Transcription

PLoS One. 2016 Aug 23;11(8):e0161360. doi: 10.1371/journal.pone.0161360. eCollection 2016.

Abstract

Measles virus (MeV) is a highly contagious virus that still causes annual epidemics in developing countries despite the availability of a safe and effective vaccine. Additionally, importation from endemic countries causes frequent outbreaks in countries where it has been eliminated. The M protein of MeV plays a key role in virus assembly and cytopathogenesis; interestingly, M is localised in nucleus, cytoplasm and membranes of infected cells. We have used transient expression of M in transfected cells and in-cell transcription assays to show that only some MeV M localizes to the nucleus, in addition to cell membranes and the cytoplasm as previously described, and can inhibit cellular transcription via binding to nuclear factors. Additionally, MeV M was able to inhibit in vitro transcription in a dose-dependent manner. Importantly, a proportion of M is also localized to nucleus of MeV infected cells at early times in infection, correlating with inhibition of cellular transcription. Our data show, for the first time, that MeV M may play a role early in infection by inhibiting host cell transcription.

MeSH terms

  • Cell Membrane / genetics
  • Cell Membrane / virology
  • Cell Nucleus / genetics
  • Chromatin / genetics
  • Chromatin / metabolism
  • Glycoproteins / genetics*
  • Glycoproteins / metabolism
  • Host-Pathogen Interactions / genetics
  • Humans
  • Measles / genetics*
  • Measles / virology
  • Measles virus / genetics*
  • Measles virus / pathogenicity
  • Protein Binding
  • Transcription Factors / genetics
  • Transcription, Genetic*
  • Viral Matrix Proteins / genetics
  • Viral Matrix Proteins / metabolism
  • Virus Assembly / genetics

Substances

  • Chromatin
  • Glycoproteins
  • Transcription Factors
  • Viral Matrix Proteins
  • protein M (glycoprotein)

Grants and funding

X.L.Y. was supported by The Shanghai Municipal Health Bureau Talents Development Foundation Grant No.: GWDTR201201.