Quantification of the virus-host interaction in human T lymphotropic virus I infection.
Quantification of the virus-host interaction in human T lymphotropic virus I infection.
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DOI：
10.1186/1742-4690-2-75
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发表时间：
2005-12-09
期刊：
影响因子：
3.3
通讯作者：
Bangham CR
中科院分区：
文献类型：
--
作者：
Asquith B;Mosley AJ;Heaps A;Tanaka Y;Taylor GP;McLean AR;Bangham CR
HTLV-I引起致残性炎症性疾病HAM/TSP：没有疫苗，没有令人满意的治疗方法，也没有评估感染者疾病风险或预后的手段。像许多具有病毒病因的免疫病理疾病一样，感染的结果被认为取决于病毒-宿主免疫相互作用。然而，病毒与宿主的动态相互作用是复杂的，目前关于HAM/TSP发病机制的模型是相互矛盾的。CD8+细胞反应被认为是HTLV-I前载量和疾病状态的决定因素，但其影响可能掩盖其他因素。我们在这里发现，在缺乏CD8+细胞的情况下，HAM/TSP患者的CD4+淋巴细胞比无症状的类似前病毒载量携带者的淋巴细胞更容易表达HTLV-I蛋白（P = 0.017）。病毒蛋白的高表达率与HAM/TSP患病率的大幅增加显著相关（P = 0.031, 89%的病例正确分类）。此外，高Tax表达率和低CD8+细胞效率与高前病毒载量独立显著相关（P = 0.005, P = 0.003）。这些结果解开了免疫监视、前病毒载量、炎症疾病和病毒蛋白表达之间的复杂关系，并表明蛋白表达升高可能在HAM/TSP发病机制中发挥重要作用。这对治疗具有重要意义，因为它表明干预措施应旨在减少税收表达，而不是原负荷本身。
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. 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). 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.
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影响因子：
4.4
作者：
Goon, PKC;Igakura, T;Bangham, CRM
通讯作者：
Bangham, CRM
影响因子：
6.4
作者：
Furukawa, Y;Yamashita, M;Osame, M
通讯作者：
Osame, M
影响因子：
3.9
作者：
INA, Y;GOJOBORI, T
通讯作者：
GOJOBORI, T
DOI：
10.1073/pnas.96.7.3848
发表时间：
1999-03-30
影响因子：
11.1
作者：
Jeffery, KJM;Usuku, K;Bangham, CRM
通讯作者：
Bangham, CRM
影响因子：
2.2
作者：
LEE, B;TANAKA, Y;TOZAWA, H
通讯作者：
TOZAWA, H