Rotavirus RNAs sponge host cell RNA binding proteins and interfere with their subcellular localization

Alfonso Oceguera1, Andrea V Peralta1, Gustavo Martínez-Delgado1

  • 1Departamento de Genética del Desarrollo y Fisiología Molecular, Instituto de Biotecnología, Universidad Nacional Autónoma de México, Cuernavaca, Morelos 62210, Mexico.

Virology
|September 26, 2018
PubMed

Insights

Rotavirus infection disrupts cellular RNA processing by causing RNA-binding proteins to relocate, disaggregate processing bodies (PBs), and accumulate in the cytoplasm. Viral RNA accumulation likely drives these changes, aiding viral replication.

Area of Science:

  • Cellular biology
  • Virology
  • Molecular biology

Background:

  • Cellular mRNAs are dynamically regulated, cycling between translation and silencing in structures like processing bodies (PBs) and GW-bodies.
  • Viruses often manipulate host cell machinery, including RNA-protein complexes, to facilitate their replication.
  • Rotavirus, a common cause of gastroenteritis, employs strategies to overcome host antiviral defenses.

Purpose of the Study:

  • To investigate how rotavirus infection alters the distribution of RNA-binding proteins and RNA granules in host cells.
  • To elucidate the mechanisms by which rotavirus counteracts cellular RNA silencing pathways.

Main Methods:

  • Analysis of RNA-binding protein distribution in rotavirus-infected cells.
  • Microscopy to observe the structural changes in processing bodies (PBs) and GW-bodies.
  • Investigating the role of viral RNA accumulation in protein redistribution.

Main Results:

  • Rotavirus infection induced the disaggregation of PBs and relocalization of GW-body proteins.
  • The predominantly nuclear protein HuR accumulated in the cytoplasm of infected cells.
  • Viral RNA accumulation in the cytoplasm is proposed as a mechanism to sequester RNA-binding proteins (RBPs).

Conclusions:

  • Rotavirus infection significantly remodels host cell RNA granules and protein localization.
  • Viral RNA acts as a potential 'RBP sponge,' sequestering host factors to promote viral replication.
  • These viral strategies contribute to successful rotavirus infection by evading host antiviral responses.

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