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Biofilm-like extracellular viral assemblies mediate HTLV-1 cell-to-cell transmission at virological synapses.类生物膜样细胞外病毒组装体在病毒突触中介导 HTLV-1 细胞间传播。
Nat Med. 2010 Jan;16(1):83-9. doi: 10.1038/nm.2065. Epub 2009 Dec 20.
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Severe loss of invariant NKT cells exhibiting anti-HTLV-1 activity in patients with HTLV-1-associated disorders.在与人类嗜T淋巴细胞病毒1型(HTLV-1)相关疾病患者中,具有抗HTLV-1活性的恒定自然杀伤T细胞严重缺失。
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Abnormally high levels of virus-infected IFN-gamma+ CCR4+ CD4+ CD25+ T cells in a retrovirus-associated neuroinflammatory disorder.在逆转录病毒相关性神经炎症疾病中,存在异常高水平的病毒感染 IFN-γ+CCR4+CD4+CD25+T 细胞。
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HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP): the role of HTLV-I-infected Th1 cells in the pathogenesis, and therapeutic strategy.人类嗜T淋巴细胞病毒I型相关脊髓病/热带痉挛性截瘫(HAM/TSP):感染人类嗜T淋巴细胞病毒I型的辅助性T细胞1在发病机制中的作用及治疗策略
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The immune control of HTLV-1 infection: selection forces and dynamics.人类嗜T淋巴细胞病毒1型(HTLV-1)感染的免疫控制:选择压力与动态变化
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PLoS Pathog. 2008 Nov;4(11):e1000205. doi: 10.1371/journal.ppat.1000205. Epub 2008 Nov 14.
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The frequency of CD127low expressing CD4+CD25high T regulatory cells is inversely correlated with human T lymphotrophic virus type-1 (HTLV-1) proviral load in HTLV-1-infection and HTLV-1-associated myelopathy/tropical spastic paraparesis.在人类嗜T淋巴细胞病毒1型(HTLV-1)感染及HTLV-1相关脊髓病/热带痉挛性截瘫中,CD127低表达的CD4+CD25高表达调节性T细胞的频率与HTLV-1前病毒载量呈负相关。
BMC Immunol. 2008 Jul 29;9:41. doi: 10.1186/1471-2172-9-41.
8
Reduced Foxp3 expression with increased cytomegalovirus-specific CTL in HTLV-I-associated myelopathy.人类嗜T淋巴细胞病毒I型相关脊髓病中Foxp3表达降低且巨细胞病毒特异性细胞毒性T淋巴细胞增加。
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9
Retrovirally induced CTL degranulation mediated by IL-15 expression and infection of mononuclear phagocytes in patients with HTLV-I-associated neurologic disease.在成人T细胞白血病病毒I型相关神经疾病患者中,由白细胞介素-15表达介导的逆转录病毒诱导的细胞毒性T淋巴细胞脱颗粒以及单核吞噬细胞的感染。
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Impaired function of human T-lymphotropic virus type 1 (HTLV-1)-specific CD8+ T cells in HTLV-1-associated neurologic disease.人类嗜T淋巴细胞病毒1型(HTLV-1)相关神经疾病中HTLV-1特异性CD8 + T细胞功能受损。
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人类嗜 T 淋巴细胞病毒 I 型感染的神经免疫。

Neuroimmunity of HTLV-I Infection.

机构信息

Viral Immunology Section, Neuroimmunology Branch, NIH, Building 10, Room 5C-103, Bethesda, MD 20892, USA.

出版信息

J Neuroimmune Pharmacol. 2010 Sep;5(3):310-25. doi: 10.1007/s11481-010-9216-9. Epub 2010 May 2.

DOI:10.1007/s11481-010-9216-9
PMID:20437106
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4765956/
Abstract

Human T-lymphotrophic virus type I (HTLV-I) is an oncogenic retrovirus and its infection is associated with a variety of human diseases including HTLV-I-associated myelopathy/tropic spastic paraparesis (HAM/TSP). Large numbers of epidemiological, virological, immunological, and clinical studies on HTLV-I- and HTLV-I-associated diseases have been published, although the pathogenesis of HAM/TSP remains to be fully understood. In the last several years, researchers have shown that several key factors are important in HTLV-I-associated neurologic disease including high HTLV-I proviral load and a strong immune response to HTLV-I. Here, we review pathophysiological findings on HAM/TSP and focus on viral-host immune responses to the virus in HTLV-I infected individuals. In particular, the role of HTLV-I-specific CD8+ T cell response is highlighted.

摘要

人类 T 淋巴细胞病毒 I 型(HTLV-I)是一种致癌逆转录病毒,其感染与多种人类疾病相关,包括 HTLV-I 相关性脊髓病/热带痉挛性截瘫(HAM/TSP)。尽管 HAM/TSP 的发病机制尚未完全阐明,但已经发表了大量关于 HTLV-I 和 HTLV-I 相关疾病的流行病学、病毒学、免疫学和临床研究。在过去的几年中,研究人员表明,几个关键因素在 HTLV-I 相关神经疾病中很重要,包括高 HTLV-I 前病毒载量和对 HTLV-I 的强烈免疫反应。在这里,我们回顾了 HAM/TSP 的病理生理学发现,并重点关注 HTLV-I 感染个体中病毒-宿主免疫反应。特别是,强调了 HTLV-I 特异性 CD8+ T 细胞反应的作用。