Gutiérrez-Millán Everardo, Rodríguez-Aguilar Eduardo Daniel, Rodríguez Mario Henry
Centre for Research in Infectious Diseases, National Institute of Public Health, Mexico.
Centre for Research in Infectious Diseases, National Institute of Public Health, Mexico.
Virology. 2025 Apr;605:110468. doi: 10.1016/j.virol.2025.110468. Epub 2025 Feb 27.
Viral diseases transmitted by insects to plants cause severe agricultural damage and arboviruses transmitted to humans cause severe disease outbreaks. The interaction between viruses and the insect defences is complex and has evolved into acting-counteracting molecular interplays. Viruses depict complex molecular mechanisms to ensure invasion, replication and exit the insect host cell, to invade other cells. On the other hand, insect cells use molecular strategies to recognize, halt replication and eliminate the invaders. In turn, virus counteract with evasive strategies. The main antiviral defence mechanism RNA interference (RNAi) recognizes and degrades viral RNA, thereby inhibiting viral replication. These in conjunction with other canonical immune pathways, Toll, IMD, JAK/STAT and Akt-ERK developed mainly to combat bacteria, fungi and protozoa, along with mechanisms to eliminate infected cells like apoptosis and phagocytosis comprise a multifactorial system. Insects exposed to an attenuated or sublethal viral infection could respond with faster and enhanced immune responses to the same pathogen (priming), which is like immunological memory in vertebrates. Several mechanisms have been proposed to explain priming, including endoreplication, epigenetic gene modifications by DNA methylation and histone acetylation. Priming could be inherited by the offspring (transgenerational immune priming, TGIP). However, the precise molecular mechanisms underlying TGIP remain to be elucidated. This article reviews the molecular mechanisms employed by insects to combat viral infections, discusses the current information and the outstanding research questions in the area.
昆虫传播给植物的病毒性疾病会造成严重的农业损害,而传播给人类的虫媒病毒会引发严重的疾病爆发。病毒与昆虫防御之间的相互作用十分复杂,已演变成相互对抗的分子相互作用。病毒展现出复杂的分子机制,以确保侵入、复制并离开昆虫宿主细胞,进而侵入其他细胞。另一方面,昆虫细胞利用分子策略来识别、阻止复制并清除入侵者。相应地,病毒则采用逃避策略。主要的抗病毒防御机制RNA干扰(RNAi)可识别并降解病毒RNA,从而抑制病毒复制。这些机制与其他主要用于对抗细菌、真菌和原生动物的经典免疫途径(Toll、IMD、JAK/STAT和Akt-ERK),以及诸如凋亡和吞噬作用等清除感染细胞的机制共同构成了一个多因素系统。暴露于减毒或亚致死性病毒感染的昆虫可能会对同一病原体产生更快、更强的免疫反应(致敏作用),这类似于脊椎动物的免疫记忆。已经提出了几种机制来解释致敏作用,包括核内复制、DNA甲基化和组蛋白乙酰化引起的表观遗传基因修饰。致敏作用可能会由后代遗传(跨代免疫致敏作用,TGIP)。然而,TGIP背后的确切分子机制仍有待阐明。本文综述了昆虫对抗病毒感染所采用的分子机制,讨论了该领域的现有信息和尚未解决的研究问题。