Modulation of alternative splicing during early infection of human primary B lymphocytes with Epstein-Barr virus (EBV): a novel function for the viral EBNA-LP protein

Nucleic Acids Res. 2021 Oct 11;49(18):10657-10676. doi: 10.1093/nar/gkab787.

Abstract

Epstein-Barr virus (EBV) is a human herpesvirus associated with human cancers worldwide. Ex vivo, the virus efficiently infects resting human B lymphocytes and induces their continuous proliferation. This process is accompanied by a global reprogramming of cellular gene transcription. However, very little is known on the impact of EBV infection on the regulation of alternative splicing, a pivotal mechanism that plays an essential role in cell fate determination and is often deregulated in cancer. In this study, we have developed a systematic time-resolved analysis of cellular mRNA splice variant expression during EBV infection of resting B lymphocytes. Our results reveal that major modifications of alternative splice variant expression appear as early as day 1 post-infection and suggest that splicing regulation provides-besides transcription-an additional mechanism of gene expression regulation at the onset of B cell activation and proliferation. We also report a role for the viral proteins, EBNA2 and EBNA-LP, in the modulation of specific alternative splicing events and reveal a previously unknown function for EBNA-LP-together with the RBM4 splicing factor-in the alternative splicing regulation of two important modulators of cell proliferation and apoptosis respectively, NUMB and BCL-X.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alternative Splicing*
  • B-Lymphocytes / virology*
  • Cells, Cultured
  • Exons
  • Herpesvirus 4, Human / physiology*
  • Humans
  • Membrane Proteins / genetics
  • RNA Splice Sites
  • RNA-Binding Proteins / metabolism
  • Viral Proteins / metabolism*
  • Viral Proteins / physiology

Substances

  • EBNA-LP protein, Human herpesvirus 4
  • Membrane Proteins
  • RNA Splice Sites
  • RNA-Binding Proteins
  • Viral Proteins