Quantification of the virus-host interaction in human T lymphotropic virus I infection
Background: 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 depen...
| मुख्य लेखकों: | , , , , , , |
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| स्वरूप: | Journal article |
| भाषा: | English |
| प्रकाशित: |
BioMed Central
2005
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| विषय: |
| _version_ | 1826267481061195776 |
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| author | Asquith, B Mosley, A Heaps, A Tanaka, Y Taylor, G McLean, A Bangham, C |
| author_facet | Asquith, B Mosley, A Heaps, A Tanaka, Y Taylor, G McLean, A Bangham, C |
| author_sort | Asquith, B |
| collection | OXFORD |
| description | Background: 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. Results: 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). Conclusion: 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 per se. |
| first_indexed | 2024-03-06T20:54:50Z |
| format | Journal article |
| id | oxford-uuid:38d5fe78-cfb8-49ed-b74d-9d8e6618e45d |
| institution | University of Oxford |
| language | English |
| last_indexed | 2024-03-06T20:54:50Z |
| publishDate | 2005 |
| publisher | BioMed Central |
| record_format | dspace |
| spelling | oxford-uuid:38d5fe78-cfb8-49ed-b74d-9d8e6618e45d2022-03-26T13:52:22ZQuantification of the virus-host interaction in human T lymphotropic virus I infectionJournal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:38d5fe78-cfb8-49ed-b74d-9d8e6618e45dImmunologyZoological sciencesEnglishOxford University Research Archive - ValetBioMed Central2005Asquith, BMosley, AHeaps, ATanaka, YTaylor, GMcLean, ABangham, CBackground: 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. Results: 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). Conclusion: 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 per se. |
| spellingShingle | Immunology Zoological sciences Asquith, B Mosley, A Heaps, A Tanaka, Y Taylor, G McLean, A Bangham, C Quantification of the virus-host interaction in human T lymphotropic virus I infection |
| title | 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_short | 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 |
| topic | Immunology Zoological sciences |
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