Imperial College London
Alternate

Dr Rob White

Faculty of Medicine, Department of Infectious Disease

Senior Lecturer
 
 
 
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Contact

 

+44 (0)20 7594 1124robert.e.white Website

 
 
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Location

 

308Norfolk PlaceSt Mary's Campus

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Summary

 

Publications

Citation

BibTex format

@article{McHugh:2017:10.1016/j.chom.2017.06.009,
author = {McHugh, D and Caduff, N and Barros, MHM and Ramer, PC and Raykova, A and Murer, A and Landtwing, V and Quast, I and Styles, CT and Spohn, M and Fowotade, A and Delecluse, H-J and Papoudou-Bai, A and Lee, Y-M and Kim, J-M and Middeldorp, J and Schulz, TF and Cesarman, E and Zbinden, A and Capaul, R and White, RE and Allday, MJ and Niedobitek, G and Blackbourn, DJ and Grundhoff, A and Munz, C},
doi = {10.1016/j.chom.2017.06.009},
journal = {Cell Host and Microbe},
pages = {61--73.e7},
title = {Persistent KSHV infection increases EBV-associated tumor formation In vivo via enhanced EBV lytic gene expression},
url = {http://dx.doi.org/10.1016/j.chom.2017.06.009},
volume = {22},
year = {2017}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - The human tumor viruses Epstein-Barr virus (EBV) and Kaposi sarcoma-associated herpesvirus (KSHV) establish persistent infections in B cells. KSHV is linked to primary effusion lymphoma (PEL), and 90% of PELs also contain EBV. Studies on persistent KSHV infection in vivo and the role of EBV co-infection in PEL development have been hampered by the absence of small animal models. We developed mice reconstituted with human immune system components as a model for KSHV infection and find that EBV/KSHV dual infection enhanced KSHV persistence and tumorigenesis. Dual-infected cells displayed a plasma cell-like gene expression pattern similar to PELs. KSHV persisted in EBV-transformed B cells and was associated with lytic EBV gene expression, resulting in increased tumor formation. Evidence of elevated lytic EBV replication was also found in EBV/KSHV dually infected lymphoproliferative disorders in humans. Our data suggest that KSHV augments EBV-associated tumorigenesis via stimulation of lytic EBV replication.
AU  - McHugh,D
AU  - Caduff,N
AU  - Barros,MHM
AU  - Ramer,PC
AU  - Raykova,A
AU  - Murer,A
AU  - Landtwing,V
AU  - Quast,I
AU  - Styles,CT
AU  - Spohn,M
AU  - Fowotade,A
AU  - Delecluse,H-J
AU  - Papoudou-Bai,A
AU  - Lee,Y-M
AU  - Kim,J-M
AU  - Middeldorp,J
AU  - Schulz,TF
AU  - Cesarman,E
AU  - Zbinden,A
AU  - Capaul,R
AU  - White,RE
AU  - Allday,MJ
AU  - Niedobitek,G
AU  - Blackbourn,DJ
AU  - Grundhoff,A
AU  - Munz,C
DO  - 10.1016/j.chom.2017.06.009
EP  - 73
PY  - 2017///
SN  - 1931-3128
SP  - 61
TI  - Persistent KSHV infection increases EBV-associated tumor formation In vivo via enhanced EBV lytic gene expression
T2  - Cell Host and Microbe
UR  - http://dx.doi.org/10.1016/j.chom.2017.06.009
UR  - http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000405309400010&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=1ba7043ffcc86c417c072aa74d649202
UR  - http://hdl.handle.net/10044/1/51663
VL  - 22
ER  -
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