Autophagy is a fundamental component of cell-autonomous immunity, targeting intracellular pathogens including viruses and cytosolic bacteria to lysosomes for degradation. Genetic mutations in components of the autophagy pathway result in autoinflammatory and neurodegenerative disorders. We focus on recent developments through the newly discovered inborn errors of autophagy strictly predisposing to severe viral infections. These feature mutations in TBK1, ATG4A, MAP1LC3B2, and ATG7, leading to herpes encephalitis, recurrent lymphocytic meningitis, and paralytic poliomyelitis. We highlight how this enhances our understanding of autophagy mechanisms and its role in human viral disease. As we better understand the contribution of these genes to disease, we can aim to develop targeted therapies for enhanced infection control.

自噬是细胞自主免疫的基本组成部分，将细胞内病原体（包括病毒和胞质细菌）靶向溶酶体进行降解。自噬通路成分的基因突变导致自身炎症和神经退行性疾病。我们通过新发现的自噬的先天性错误来关注最近的发展，这些错误严格易患严重的病毒感染。这些特征突变在TBK1、ATG4A、MAP1LC3B2和ATG7，导致疱疹性脑炎、复发性淋巴细胞性脑膜炎和麻痹性脊髓灰质炎。我们强调这如何增强我们对自噬机制及其在人类病毒性疾病中的作用的理解。随着我们更好地了解这些基因对疾病的贡献，我们可以致力于开发靶向疗法以增强感染控制。