Quantification of the virus-host interaction in human T lymphotropic virus I infection
<p>Abstract</p> <p>Background</p> <p>HTLV-I causes the disabling inflammatory disease HAM/TSP: there is no vaccine, no satisfactory treatment and no means of assessing the risk of disease or prognosis in infected people. Like many immunopathological diseases with a vira...
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doaj-1a3c4c5eefc94b84bde41200fd7e0e532020-11-25T01:08:00ZengBMCRetrovirology1742-46902005-12-01217510.1186/1742-4690-2-75Quantification of the virus-host interaction in human T lymphotropic virus I infectionTaylor Graham PTanaka YuetsuHeaps AdrianMosley Angelina JAsquith BeccaMcLean Angela RBangham Charles RM<p>Abstract</p> <p>Background</p> <p>HTLV-I causes the disabling inflammatory disease HAM/TSP: there is no vaccine, no satisfactory treatment and no means of assessing the risk of disease or prognosis in infected people. Like many immunopathological diseases with a viral etiology the outcome of infection is thought to depend on the virus-host immunology interaction. However the dynamic virus-host interaction is complex and current models of HAM/TSP pathogenesis are conflicting. The CD8+ cell response is thought to be a determinant of both HTLV-I proviral load and disease status but its effects can obscure other factors.</p> <p>Results</p> <p>We show here that in the absence of CD8+ cells, CD4+ lymphocytes from HAM/TSP patients expressed HTLV-I protein significantly more readily than lymphocytes from asymptomatic carriers of similar proviral load (P = 0.017). A high rate of viral protein expression was significantly associated with a large increase in the prevalence of HAM/TSP (P = 0.031, 89% of cases correctly classified). Additionally, a high rate of Tax expression and a low CD8+ cell efficiency were independently significantly associated with a high proviral load (P = 0.005, P = 0.003 respectively).</p> <p>Conclusion</p> <p>These results disentangle the complex relationship between immune surveillance, proviral load, inflammatory disease and viral protein expression and indicate that increased protein expression may play an important role in HAM/TSP pathogenesis. This has important implications for therapy since it suggests that interventions should aim to reduce Tax expression rather than proviral load <it>per se</it>.</p> http://www.retrovirology.com/content/2/1/75 |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Taylor Graham P Tanaka Yuetsu Heaps Adrian Mosley Angelina J Asquith Becca McLean Angela R Bangham Charles RM |
spellingShingle |
Taylor Graham P Tanaka Yuetsu Heaps Adrian Mosley Angelina J Asquith Becca McLean Angela R Bangham Charles RM Quantification of the virus-host interaction in human T lymphotropic virus I infection Retrovirology |
author_facet |
Taylor Graham P Tanaka Yuetsu Heaps Adrian Mosley Angelina J Asquith Becca McLean Angela R Bangham Charles RM |
author_sort |
Taylor Graham P |
title |
Quantification of the virus-host interaction in human T lymphotropic virus I infection |
title_short |
Quantification of the virus-host interaction in human T lymphotropic virus I infection |
title_full |
Quantification of the virus-host interaction in human T lymphotropic virus I infection |
title_fullStr |
Quantification of the virus-host interaction in human T lymphotropic virus I infection |
title_full_unstemmed |
Quantification of the virus-host interaction in human T lymphotropic virus I infection |
title_sort |
quantification of the virus-host interaction in human t lymphotropic virus i infection |
publisher |
BMC |
series |
Retrovirology |
issn |
1742-4690 |
publishDate |
2005-12-01 |
description |
<p>Abstract</p> <p>Background</p> <p>HTLV-I causes the disabling inflammatory disease HAM/TSP: there is no vaccine, no satisfactory treatment and no means of assessing the risk of disease or prognosis in infected people. Like many immunopathological diseases with a viral etiology the outcome of infection is thought to depend on the virus-host immunology interaction. However the dynamic virus-host interaction is complex and current models of HAM/TSP pathogenesis are conflicting. The CD8+ cell response is thought to be a determinant of both HTLV-I proviral load and disease status but its effects can obscure other factors.</p> <p>Results</p> <p>We show here that in the absence of CD8+ cells, CD4+ lymphocytes from HAM/TSP patients expressed HTLV-I protein significantly more readily than lymphocytes from asymptomatic carriers of similar proviral load (P = 0.017). A high rate of viral protein expression was significantly associated with a large increase in the prevalence of HAM/TSP (P = 0.031, 89% of cases correctly classified). Additionally, a high rate of Tax expression and a low CD8+ cell efficiency were independently significantly associated with a high proviral load (P = 0.005, P = 0.003 respectively).</p> <p>Conclusion</p> <p>These results disentangle the complex relationship between immune surveillance, proviral load, inflammatory disease and viral protein expression and indicate that increased protein expression may play an important role in HAM/TSP pathogenesis. This has important implications for therapy since it suggests that interventions should aim to reduce Tax expression rather than proviral load <it>per se</it>.</p> |
url |
http://www.retrovirology.com/content/2/1/75 |
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