Club cells surviving influenza A virus infection induce temporary nonspecific antiviral immunity
Club cells surviving influenza A virus infection induce temporary nonspecific antiviral immunity
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DOI：
10.1073/pnas.1522376113
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发表时间：
2016-04-05
影响因子：
11.1
通讯作者：
Heaton, Nicholas S.
中科院分区：
文献类型：
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作者：
Hamilton, Jennifer R.;Sachs, David;Heaton, Nicholas S.
甲型流感病毒 (IAV) 感染后观察到短暂的抗原非特异性保护窗口。尽管这种暂时的免疫被认为是残留的非特异性炎症的结果，但这段诱导免疫的时期尚未得到充分研究。由于 IAV 长期以来一直被认为是一种细胞病变病毒（基于其能够快速裂解培养物中大多数细胞类型的能力），因此直接感染的细胞不会产生这种效应已成为既定的结论。使用表达 Cre 重组酶的 IAV，我们之前已经证明俱乐部细胞可以在直接病毒感染中存活。我们在这里表明，这些细胞不仅可以消除所有病毒痕迹并存活下来，而且它们在存活后获得了增强的抗病毒反应表型。此外，我们通过实验证明了 IAV 感染后的临时非特异性病毒免疫，并表明这种表型需要存活细胞。这项工作描述了病毒诱导的先天免疫反应调节，这可能代表了预防病毒性疾病的新机制。
A brief window of antigen-nonspecific protection has been observed after influenza A virus (IAV) infection. Although this temporary immunity has been assumed to be the result of residual nonspecific inflammation, this period of induced immunity has not been fully studied. Because IAV has long been characterized as a cytopathic virus (based on its ability to rapidly lyse most cell types in culture), it has been a forgone conclusion that directly infected cells could not be contributing to this effect. Using a Cre recombinase-expressing IAV, we have previously shown that club cells can survive direct viral infection. We show here not only that these cells can eliminate all traces of the virus and survive but also that they acquire a heightened antiviral response phenotype after surviving. Moreover, we experimentally demonstrate temporary nonspecific viral immunity after IAV infection and show that surviving cells are required for this phenotype. This work characterizes a virally induced modulation of the innate immune response that may represent a new mechanism to prevent viral diseases.