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细小病毒B19非结构(NS1)蛋白作为白细胞介素-6合成的反式激活因子:人类细小病毒感染炎症后遗症的共同途径?

Parvovirus B19 nonstructural (NS1) protein as a transactivator of interleukin-6 synthesis: common pathway in inflammatory sequelae of human parvovirus infections?

作者信息

Mitchell Leslie Ann

机构信息

Department of Pathology, University of British Columbia, Vancouver, Canada.

出版信息

J Med Virol. 2002 Jun;67(2):267-74. doi: 10.1002/jmv.2217.

Abstract

This review focuses on the role that human parvovirus B19 nonstructural (NS1) protein as a transactivator of the proinflammatory cytokine, interleukin-6 (IL-6), might play in triggering the multiparametric inflammatory outcomes of B19 infection. Parvovirus B19 is a ubiquitous virus, and it is often expressed during conditions of immunodepression including that induced by long-term chemotherapy, viral infection (HIV, HTLV-1), or genetic immunodeficiency disorders. Through NS1 expression, B19 may contribute to the immune dysregulation associated with these disorders, or serve as a cofactor in enhancing retroviral replication. Hence, NS1 transactivation of proinflammatory cytokine promoters such as IL-6 may be pivotal in triggering the various inflammatory and autoimmune disorders that have been linked to parvovirus B19 infections.

摘要

本综述聚焦于人类细小病毒B19非结构(NS1)蛋白作为促炎细胞因子白细胞介素-6(IL-6)的反式激活因子,在引发B19感染的多参数炎症反应中可能发挥的作用。细小病毒B19是一种普遍存在的病毒,常在免疫抑制状态下表达,包括长期化疗、病毒感染(HIV、HTLV-1)或遗传性免疫缺陷疾病所诱导的免疫抑制。通过NS1的表达,B19可能促成与这些疾病相关的免疫失调,或作为增强逆转录病毒复制的辅助因子。因此,NS1对诸如IL-6等促炎细胞因子启动子的反式激活,可能在引发与细小病毒B19感染相关的各种炎症和自身免疫性疾病中起关键作用。

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