RIG-I-like receptors (RLRs) are cytoplasmic sensors of viral RNA that trigger the signaling cascade that leads to type I interferon (IFN) production. Transcriptional induction of RLRs by IFN is believed to play the role of positive feedback to further amplify viral sensing. We found that RLRs and several other IFN-stimulated genes (ISGs) are induced early in viral infection independent of IFN. Expression of these early ISGs requires IRF3/IRF7 and is highly correlated amongst them. Simultaneous detection of mRNA of IFNB1, viral replicase, and ISGs revealed distinct populations of IFNB1 expressing and non-expressing cells which are highly correlated with the levels of early ISGs but are uncorrelated with IFN-dependent ISGs and viral gene expression. Individual expression of RLRs made IFNB1 expression more robust and earlier, suggesting a causal relation between levels of RLR and induction of IFN.

中文翻译：

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早期抗病毒基因表达的单细胞分析揭示了随机 IFNB1 表达的决定因素


RIG-I 样受体 (RLR) 是病毒 RNA 的细胞质传感器，可触发信号级联反应，从而导致 I 型干扰素 (IFN) 的产生。 IFN 对 RLR 的转录诱导被认为发挥正反馈作用，进一步放大病毒感应。我们发现 RLR 和其他几个 IFN 刺激基因 (ISG) 在病毒感染早期被诱导，与 IFN 无关。这些早期 ISG 的表达需要 IRF3/IRF7，并且它们之间高度相关。同时检测 IFNB1、病毒复制酶和 ISG 的 mRNA 揭示了不同的 IFNB1 表达和非表达细胞群体，这些细胞与早期 ISG 的水平高度相关，但与 IFN 依赖性 ISG 和病毒基因表达不相关。 RLR 的个体表达使 IFNB1 的表达更加强烈和更早，表明 RLR 水平与 IFN 诱导之间存在因果关系。