Imperial College London
ANAT MELAMED

ANAT MELAMED

Faculty of Medicine, Department of Infectious Disease

Research Associate
 
 
 
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Contact

 

anat.melamed07

 
 
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Location

 

VD1Medical SchoolSt Mary's Campus

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Summary

 

Publications

Citation

BibTex format

@article{Melamed:2014:10.1371/journal.ppat.1004006,
author = {Melamed, A and Witkover, AD and Laydon, DJ and Brown, R and Ladell, K and Miners, K and Rowan, AG and Gormley, N and Price, DA and Taylor, GP and Murphy, EL and Bangham, CRM},
doi = {10.1371/journal.ppat.1004006},
journal = {PLoS Pathogens},
pages = {1--9},
title = {Clonality of HTLV-2 in natural infection},
url = {http://dx.doi.org/10.1371/journal.ppat.1004006},
volume = {10},
year = {2014}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - Human T-lymphotropic virus type 1 (HTLV-1) and type 2 (HTLV-2) both cause lifelong persistent infections, but differ in their clinical outcomes. HTLV-1 infection causes a chronic or acute T-lymphocytic malignancy in up to 5% of infected individuals whereas HTLV-2 has not been unequivocally linked to a T-cell malignancy. Virus-driven clonal proliferation of infected cells both in vitro and in vivo has been demonstrated in HTLV-1 infection. However, T-cell clonality in HTLV-2 infection has not been rigorously characterized. In this study we used a high-throughput approach in conjunction with flow cytometric sorting to identify and quantify HTLV-2-infected T-cell clones in 28 individuals with natural infection. We show that while genome-wide integration site preferences in vivo were similar to those found in HTLV-1 infection, expansion of HTLV-2-infected clones did not demonstrate the same significant association with the genomic environment of the integrated provirus. The proviral load in HTLV-2 is almost confined to CD8+ T-cells and is composed of a small number of often highly expanded clones. The HTLV-2 load correlated significantly with the degree of dispersion of the clone frequency distribution, which was highly stable over ∼8 years. These results suggest that there are significant differences in the selection forces that control the clonal expansion of virus-infected cells in HTLV-1 and HTLV-2 infection. In addition, our data demonstrate that strong virus-driven proliferation per se does not predispose to malignant transformation in oncoretroviral infections.
AU  - Melamed,A
AU  - Witkover,AD
AU  - Laydon,DJ
AU  - Brown,R
AU  - Ladell,K
AU  - Miners,K
AU  - Rowan,AG
AU  - Gormley,N
AU  - Price,DA
AU  - Taylor,GP
AU  - Murphy,EL
AU  - Bangham,CRM
DO  - 10.1371/journal.ppat.1004006
EP  - 9
PY  - 2014///
SN  - 1553-7366
SP  - 1
TI  - Clonality of HTLV-2 in natural infection
T2  - PLoS Pathogens
UR  - http://dx.doi.org/10.1371/journal.ppat.1004006
UR  - http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000337470300048&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=1ba7043ffcc86c417c072aa74d649202
UR  - https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1004006
UR  - http://hdl.handle.net/10044/1/21226
VL  - 10
ER  -
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