Contribution of Epstein⁻Barr Virus Latent Proteins to the Pathogenesis of Classical Hodgkin Lymphoma

Research output: Contribution to journalReview article

Authors

External organisations

  • Institute for Cancer and Genomic Medicine, University of Birmingham, Birmingham B15 2TT, UK. k.vrzalikova@bham.ac.uk.
  • Institute for Cancer and Genomic Medicine, University of Birmingham, Birmingham B15 2TT, UK. taosun77@gmail.com.
  • Institute of Immunology and Immunotherapy, University of Birmingham, Birmingham B15 2TT, UK. g.m.reynolds@bham.ac.uk.
  • Institute for Cancer and Genomic Medicine, University of Birmingham, Birmingham B15 2TT, UK. p.g.murray@bham.ac.uk.
  • Department of Clinical and Molecular Pathology, Institute of Molecular and Translational Medicine, Faculty of Medicine and Dentistry, Palacky University, 775 15 Olomouc, Czech Republic. p.g.murray@bham.ac.uk.

Abstract

Pathogenic viruses have evolved to manipulate the host cell utilising a variety of strategies including expression of viral proteins to hijack or mimic the activity of cellular functions. DNA tumour viruses often establish latent infection in which no new virions are produced, characterized by the expression of a restricted repertoire of so-called latent viral genes. These latent genes serve to remodel cellular functions to ensure survival of the virus within host cells, often for the lifetime of the infected individual. However, under certain circumstances, virus infection may contribute to transformation of the host cell; this event is not a usual outcome of infection. Here, we review how the Epstein⁻Barr virus (EBV), the prototypic oncogenic human virus, modulates host cell functions, with a focus on the role of the EBV latent genes in classical Hodgkin lymphoma.

Details

Original languageEnglish
Article number59
JournalPathogens
Volume7
Issue number3
Publication statusPublished - 27 Jun 2018

Keywords

  • Epstein–Barr virus, Hodgkin lymphoma, latency, B cells