Varicella zoster virus immune evasion strategies.

Varicella zoster virus immune evasion strategies.
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DOI:
10.1007/82_2010_41
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发表时间:
2010
影响因子:
--
通讯作者:
Slobedman, Barry
Slobedman, Barry
中科院分区:
医学3区
文献类型:
--
作者:
Abendroth, Allison;Kinchington, Paul R.;Slobedman, Barry

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水痘带状疱疹病毒(VZV)通过多个步骤引起水痘(水痘)的能力,首先是在宿主的粘膜部位用呼吸道飞沫中的传染性病毒进行接种。尽管存在强大的免疫防御系统,该病毒仍能够从最初感染部位传播到多个部位,导致出现独特的皮肤水疱脓疱性病变。最近,有人提出,导致皮肤感染的步骤包括 VZV 感染人扁桃体 CD4+ T 细胞,这些细胞表达皮肤归巢标记,使它们能够在原发性病毒血症期间将 VZV 从淋巴结直接转运到皮肤。还有人提出,呼吸道粘膜的树突状细胞(DC)可能是最先遇到水痘带状疱疹病毒的细胞之一,这些细胞可能会将病毒转运至引流淋巴结。这些不同的病毒与宿主细胞的相互作用都需要在完整的宿主免疫反应的情况下发生,病毒才能成功引起疾病。值得注意的是,初次暴露于水痘带状疱疹病毒后,出现皮肤损伤之前有一段较长的潜伏期,在此期间适应性免疫反应被延迟。出于这些原因,有人提出,VZV 必须编码通过逃避免疫反应而使病毒受益的功能。本章将回顾迄今为止发现的多种免疫调节机制,VZV 已经进化到至少暂时限制免疫识别。
The capacity of varicella zoster virus (VZV) to cause varicella (chickenpox) relics upon multiple steps, beginning with inoculation of the host at mucosal sites with infectious virus in respiratory droplets. Despite the presence of a powerful immune defense system, this virus is able to disseminate from the site of initial infection to multiple sites, resulting in the emergence of distinctive cutaneous vesiculopustular lesions. Most recently, it has been proposed that the steps leading to cutaneous infection include VZV infecting human tonsillar CD4+ T cells that express skin homing markers that allow them to transport VZV directly from the lymph node to the skin during the primary viremia. It has also been proposed that dendritic cells (DC) of the respiratory mucosa may be among the first cells to encounter VZV and these cells may transport virus to the draining lymph node. These various virus-host cell interactions would all need to occur in the face of an intact host immune response for the virus to successfully cause disease. Significantly, following primary exposure to VZV, there is a prolonged incubation period before emergence of skin lesions, during which time the adaptive immune response is delayed. For these reasons, it has been proposed that VZV must encode functions which benefit the virus by evading the immune response. This chapter will review the diverse array of immunomodulatory mechanisms identified to date that VZV has evolved to at least transiently limit immune recognition.
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