Imperial College London
Alternate

ProfessorCharlesBangham

Institute of Infection

Co-Director of the Institute of Infection
 
 
 
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Contact

 

+44 (0)20 7594 3730c.bangham Website

 
 
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Assistant

 

Ms Linda Hollick +44 (0)20 7594 3729

 
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Location

 

115Wright Fleming WingSt Mary's Campus

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Summary

 

Publications

Citation

BibTex format

@unpublished{Laydon:2019:10.1101/799197,
author = {Laydon, DJ and Sunkara, V and Boelen, L and Bangham, CRM and Asquith, B},
doi = {10.1101/799197},
title = {The relative contributions of infectious and mitotic spread to HTLV-1 persistence},
url = {http://dx.doi.org/10.1101/799197},
year = {2019}
}
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RIS format (EndNote, RefMan)

TY  - UNPB
AB  - <jats:title>Abstract</jats:title><jats:p>Human T-lymphotropic virus type-1 (HTLV-1) persists within hosts via infectious spread (<jats:italic>de novo</jats:italic>infection) and mitotic spread (infected cell proliferation), creating a population structure of multiple clones (infected cell populations with identical genomic proviral integration sites). The relative contributions of infectious and mitotic spread to HTLV-1 persistence are unknown, and will determine the efficacy of different approaches to treatment.</jats:p><jats:p>The prevailing view is that infectious spread is negligible in HTLV-1 proviral load maintenance beyond early infection. However, in light of recent high-throughput data on the abundance of HTLV-1 clones, and recent estimates of HTLV-1 clonal diversity that are substantially higher than previously thought (typically between 10<jats:sup>4</jats:sup>and 10<jats:sup>5</jats:sup>HTLV-1<jats:sup>+</jats:sup>T cell clones in the body of an asymptomatic carrier or patient with HAM/TSP), ongoing infectious spread during chronic infection remains possible.</jats:p><jats:p>We estimate the ratio of infectious to mitotic spread using a hybrid model of deterministic and stochastic processes, fitted to previously published HTLV-1 clonal diversity estimates. We investigate the robustness of our estimates using two alternative methods. We find that, contrary to previous belief, infectious spread persists during chronic infection, even after HTLV-1 proviral load has reached its set point, and we estimate that between 100 and 200 new HTLV-1 clones are created and killed every day. We find broad agreement between all three methods.</jats:p><jats:p>The risk of HTLV-1-associated malignancy and inflammatory disease is strongly correlated with proviral load, which in turn is correlated with the number of HTLV-1-infected clones, which are created by de novo infectio
AU  - Laydon,DJ
AU  - Sunkara,V
AU  - Boelen,L
AU  - Bangham,CRM
AU  - Asquith,B
DO  - 10.1101/799197
PY  - 2019///
TI  - The relative contributions of infectious and mitotic spread to HTLV-1 persistence
UR  - http://dx.doi.org/10.1101/799197
ER  -
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