Abstract

Most of the world’s population is infected by the Epstein–Barr virus (EBV), but the incidence of the diseases associated with EBV infection differs greatly in different parts of the world. Many factors may determine those differences, but variation in the virus genome is likely to be a contributing factor for some of the diseases. Here, we describe the main forms of EBV genome sequence variation, and the mechanisms by which variations in the virus genome are likely to contribute to disease. EBV genome deletions or polymorphisms can also provide useful markers for monitoring disease. If some EBV strains prove to be more pathogenic than others, this suggests the possible value of immunising people against infection by those pathogenic strains.

Highlights

  • Most of the world’s population is infected by the Epstein–Barr virus (EBV), but the incidence of the diseases associated with EBV infection differs greatly in different parts of the world

  • EBV strains prove to be more pathogenic than others, this suggests the possible value of immunising people against infection by those pathogenic strains

  • EBV single nucleotide polymorphism (SNP) in Zp known as V3 results in the stronger activation of BZLF1 because it creates an extra binding site for the cell NF-AT transcription factor [21], which is activated by BCR signal transduction

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Summary

Epstein–Barr Virus Biology

Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. For EBV, transmission is via saliva transfer (for example, in kissing), with the virus perhaps briefly replicating in epithelial cells in the mouth or throat. This gives access to the main target cells, which are B lymphocytes, most likely encountered in the tonsils or other lymphoid organs in the oropharynx. People shed highly variable levels of infectious virus in their saliva over time [2] and maintain a long-term immune response, including antibodies to the EBNA1 viral protein and memory T cells that can target several EBV antigens. The abilities of EBV gene products to cause cell proliferation, prevent apoptosis or evade immunity link the virus to some of these diseases. This article will focus on the significance of diseases caused by variations and alterations in the EBV genome

Natural Variation in the EBV Genome
Type 1 and Type 2 EBV
Geographic and Ethnic Variation in EBV Genome Sequence
Schematic
Immune Deficiency in EBV-Associated Diseases
Burkitt Lymphoma
Hodgkin Lymphoma
Carcinomas Associated with EBV
Incidence
Vaccines to Prevent Diseases Associated with EBV
Findings
Conclusions
Full Text
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