Quantification of the virus-host interaction in human T lymphotropic virus I infection
Autor: | Graham P. Taylor, Yuetsu Tanaka, Charles R. M. Bangham, Angelina J. Mosley, Becca Asquith, Angela R. McLean, Adrian Heaps |
---|---|
Jazyk: | angličtina |
Rok vydání: | 2016 |
Předmět: |
HTLV-1-ASSOCIATED MYELOPATHY
Cell NEUROLOGIC DISEASE Disease LYMPHOCYTES medicine.disease_cause Zoological sciences Pathogenesis 0302 clinical medicine Proviruses immune system diseases GENE-EXPRESSION 0303 health sciences biology virus diseases Gene Products tax Middle Aged Viral Load 3. Good health Infectious Diseases medicine.anatomical_structure Carrier State Antibody Life Sciences & Biomedicine Viral load Adult lcsh:Immunologic diseases. Allergy Viral protein PROVIRAL LOAD Immunology PERIPHERAL-BLOOD 03 medical and health sciences Virology TAX PROTEIN medicine Humans RNA Messenger Aged 030304 developmental biology Science & Technology Research 1103 Clinical Sciences HTLV-I HTLV-I Infections CD4 Lymphocyte Count biology.protein TROPICAL SPASTIC PARAPARESIS lcsh:RC581-607 Asymptomatic carrier CD8 CELL LEUKEMIA-VIRUS T-Lymphocytes Cytotoxic 030215 immunology |
Zdroj: | Retrovirology, Vol 2, Iss 1, p 75 (2005) Retrovirology |
DOI: | 10.1186/1742-4690-2-75 |
Popis: | BackgroundHTLV-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.ResultsWe 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).ConclusionThese 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 loadper se. |
Databáze: | OpenAIRE |
Externí odkaz: |