Apoptosis and autophagy are two most prominent forms of programmed cell deaths (PCD) that have been implicated in antiviral immunity in vertebrate and plant hosts. Arboviruses are able to coexist with its arthropod vectors by coordinating the PCD immunity, but the regulatory mechanism involved is largely unknown. We found that the coat protein (CP) of an insect-borne plant virus TYLCV directly interacted with a phosphatidylethanolamine-binding protein (PEBP) of its insect vector whitefly to negatively influence the MAPK signaling cascade. As a result, the apoptosis was activated in whitefly which increased viral loading. Simultaneously, the PEBP4-CP interaction liberated ATG8, the hallmark of autophagy initiation, and eliminates arbovirus. Furthermore, apoptosis-promoted virus loading was compromised by agonist-induced autophagy, but autophagy-associated suppression on virus loading was unaffected by apoptosis agonist or inhibitor, suggesting that virus loading was predominantly determined by autophagy rather than by apoptosis. Our results demonstrated that maintaining a mild immune response by coordinating apoptosis and autophagy processes presumably could facilitate coexistence of the arbovirus and its insect vector. Taken together, immune homeostasis shaped by two types of PCD may facilitate the arbovirus preservation within the insect vector.

中文翻译：

---

PEBP调节凋亡和自噬之间的平衡，使虫媒病毒和昆虫载体共存

凋亡和自噬是程序性细胞死亡（PCD）的两种最主要形式，它们与脊椎动物和植物宿主的抗病毒免疫有关。虫媒病毒能够通过协调PCD免疫力与其节肢动物载体共存，但所涉及的调节机制尚不清楚。我们发现昆虫传播的植物病毒TYLCV的外壳蛋白（CP）直接与其昆虫载体粉虱的磷脂酰乙醇胺结合蛋白（PEBP）相互作用，从而对MAPK信号级联反应产生负面影响。结果，在粉虱中激活了细胞凋亡，这增加了病毒载量。同时，PEBP4-CP相互作用释放了自噬起始的标志物ATG8，并消除了虫媒病毒。此外，激动剂诱导的自噬损害了细胞凋亡促进的病毒载量，但是自噬相关的病毒载量抑制不受凋亡激动剂或抑制剂的影响，这表明病毒载量主要由自噬而不是凋亡决定。我们的结果表明，通过协调细胞凋亡和自噬过程来维持轻度的免疫反应大概可以促进虫媒病毒及其昆虫载体的共存。综上所述，由两种类型的PCD形成的免疫稳态可以促进虫媒病毒在昆虫载体中的保存。我们的结果表明，通过协调细胞凋亡和自噬过程来维持轻度的免疫反应大概可以促进虫媒病毒及其昆虫载体的共存。综上所述，由两种类型的PCD形成的免疫稳态可以促进虫媒病毒在昆虫载体中的保存。我们的结果表明，通过协调细胞凋亡和自噬过程来维持轻度的免疫反应大概可以促进虫媒病毒及其昆虫载体的共存。综上所述，由两种类型的PCD形成的免疫稳态可以促进虫媒病毒在昆虫载体中的保存。