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Herpesvirus latency confers symbiotic protection from bacterial infection

机译：疱疹病毒潜伏期使共生保护免受细菌感染

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摘要

All humans become infected with multiple herpesviruses during childhood. After clearance of acute infection, herpesviruses enter a dormant state known as latency. Latency persists for the life of the host and is presumed to be parasitic, as it leaves the individual at risk for subsequent viral reactivation and disease. Here we show that herpesvirus latency also confers a surprising benefit to the host. Mice latently infected with either murine gammaherpes-virus 68 or murine cytomegalovirus, which are genetically highly similar to the human pathogens Epstein-Barr virus and human cytomegalovirus, respectively, are resistant to infection with the bacterial pathogens Listeria monocytogenes and Yersinia pestis. Latency-induced protection is not antigen specific but involves prolonged production of the antiviral cytokine interferon-γ and systemic activation of macrophages. Latency thereby upregulates the basal activation state of innate immunity against subsequent infections. We speculate that herpesvirus latency may also sculpt the immune response to self and environmental antigens through establishment of a polarized cytokine environment. Thus, whereas the immune evasion capabilities and lifelong persistence of herpesviruses are commonly viewed as solely pathogenic, our data suggest that latency is a symbiotic relationship with immune benefits for the host.
机译：所有人类在童年时期都感染了多种疱疹病毒。清除急性感染后，疱疹病毒进入休眠状态，称为潜伏期。潜伏期一直持续到宿主的整个生命周期，并被认为是寄生的，因为它使个体处于随后发生病毒再激活和疾病的危险中。在这里，我们显示疱疹病毒潜伏期也为宿主带来了令人惊讶的好处。潜伏性感染鼠γ-疱疹病毒68或鼠巨细胞病毒的小鼠，在基因上分别与人类病原体爱泼斯坦-巴尔病毒和人类巨细胞病毒高度相似，它们对细菌病原体李斯特菌和鼠疫耶尔森氏菌的感染具有抵抗力。延迟诱导的保护不是抗原特异性的，而是涉及抗病毒细胞因子干扰素-γ的延长产生和巨噬细胞的全身活化。延迟从而上调了针对后续感染的先天免疫的基础激活状态。我们推测，疱疹病毒潜伏期还可能通过建立极化细胞因子环境来塑造对自身和环境抗原的免疫反应。因此，尽管疱疹病毒的免疫逃避能力和终生持久性通常被视为仅是致病性的，但我们的数据表明潜伏期与宿主的免疫益处是共生关系。

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