The cell-autonomous innate immune system enables animal cells to resist viral infection. This system comprises an array of sensors that, after detecting viral molecules, activate the expression of antiviral proteins and the interferon response. The repertoire of immune sensors and antiviral proteins has long been considered to be derived from extensive evolutionary innovation in vertebrates, but new data challenge this dogma. Recent studies show that central components of the cell-autonomous innate immune system have ancient evolutionary roots in prokaryotic genes that protect bacteria from phages. These include the cyclic GMP–AMP synthase (cGAS)–stimulator of interferon genes (STING) pathway, Toll/IL-1 receptor (TIR) domain-containing pathogen receptors, the viperin family of antiviral proteins, SAMHD1-like nucleotide-depletion enzymes, gasdermin proteins and key components of the RNA interference pathway. This Perspective details current knowledge of the elements of antiviral immunity that are conserved from bacteria to humans, and presents possible evolutionary scenarios to explain the observed conservation.

细胞自主的先天免疫系统使动物细胞能够抵抗病毒感染。该系统包括一系列传感器，这些传感器在检测到病毒分子后，会激活抗病毒蛋白的表达和干扰素反应。长期以来，免疫传感器和抗病毒蛋白的所有组成部分一直被认为源自脊椎动物的广泛进化创新，但新的数据挑战了这一教条。最近的研究表明，细胞自主先天免疫系统的核心成分在保护细菌免受噬菌体侵害的原核基因中具有古老的进化根源。这些包括环状 GMP-AMP 合酶 (cGAS) - 干扰素基因刺激物 (STING) 途径、含有 Toll/IL-1 受体 (TIR) 结构域的病原体受体、抗病毒蛋白 viperin 家族、SAMHD1 样核苷酸消耗酶, gasdermin 蛋白和 RNA 干扰途径的关键成分。该观点详细介绍了从细菌到人类的抗病毒免疫元素的当前知识，并提出了可能的进化情景来解释观察到的保护。