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Epstein-Barr virus genome deletions in Epstein-Barr virus-positive T/NK cell lymphoproliferative diseases
File(s)
jvi.00394-22.pdf (1.81 MB)
Published version
Author(s)
Wongwiwat, Wiyada
Fournier, Benjamin
Bassano, Irene
Bayoumy, Amr
Elgueta Karstegl, Claudio
Type
Journal Article
Abstract
The main target cells for Epstein-Barr virus (EBV) infection and persistence are B lymphocytes, although T and NK cells can also become infected. In this paper we characterise the EBV present in 21 pediatric and adult patients treated in France for a range of diseases that involve infection of T or NK cells. Of these 21 cases, 5 pediatric patients (21%) and 11 adult patients (52%) are of Caucasian origin. In about 30% of the cases, some of the EBV genomes contain a large deletion. The deletions are different in every patient but tend to cluster near the BART region of the viral genome. Detailed investigation of a family, in which several members have persistent T or NK cell infection by EBV, indicates that the virus genome deletions arise or are selected independently in each individual patient. Genome sequence polymorphisms in the EBV in these T or NK cell diseases reflect the geographic origin of the patient, not a distinct type of EBV (the 21 cases studied included examples of both type 1 and type 2 EBV infection). Using virus produced from type 1 or type 2 EBV genomes cloned in bacterial artificial chromosome (BAC) vectors, we demonstrate infection of T cells in cord blood from healthy donors. Our results are consistent with transient infection of some T cells being part of normal asymptomatic infection by EBV in young children.
Date Issued
2022-06
Date Acceptance
2022-05-03
Citation
Journal of Virology, 2022, 96 (12), pp.1-15
URI
URL
DOI
ISSN
0022-538X
Publisher
American Society for Microbiology
Start Page
1
End Page
15
Journal / Book Title
Journal of Virology
Volume
96
Issue
12
Copyright Statement
© 2022 Wongwiwat et al. This is an
open-access article distributed under the terms
of the Creative Commons Attribution 4.0
International license
License URL
Identifier
https://journals.asm.org/doi/epub/10.1128/jvi.00394-22
Publication Status
Published
Date Publish Online
2022-05-25