Viroporins are virus encoded proteins that alter membrane permeability and can trigger subsequent cellular signals. Oligomerization of viroporin subunits results in formation of a hydrophilic pore which facilitates ion transport across host cell membranes. These viral channel proteins may be involved in different stages of the virus infection cycle. Inflammasomes are large multimolecular complexes best recognized for their ability to control activation of caspase-1, which in turn regulates the maturation of interleukin-1 β (IL-1β) and interleukin 18 (IL-18). IL-1β was originally identified as a pro-inflammatory cytokine able to induce both local and systemic inflammation and a febrile reaction in response to infection or injury. Excessive production of IL-1β is associated with autoimmune and inflammatory diseases. Microbial derivatives, bacterial pore-forming toxins, extracellular ATP and other pathogen-associated molecular patterns trigger activation of NLRP3 inflammasomes. Recent studies have reported that viroporin activity is capable of inducing inflammasome activity and production of IL-1β, where NLRP3 is shown to be regulated by fluxes of K⁺, H⁺ and Ca²⁺ in addition to reactive oxygen species, autophagy and endoplasmic reticulum stress. The aim of this review is to present an overview of the key findings on viroporin activity with special emphasis on their role in virus immunity and as possible activators of inflammasomes.

Viroporin是病毒编码的蛋白，可改变膜的通透性并触发随后的细胞信号。viroporin亚基的低聚导致亲水孔的形成，这有助于离子跨宿主细胞膜的运输。这些病毒通道蛋白可能参与病毒感染周期的不同阶段。炎性小体是大型多分子复合物，因其控制caspase-1激活的能力而广为人知，而caspase-1的激活又调节白介素1β（IL-1β）和白介素18（IL-18）的成熟。IL-1β最初被鉴定为促炎性细胞因子，能够诱导局部和全身性炎症，并对感染或损伤产生发热反应。IL-1β的过量产生与自身免疫性疾病和炎性疾病有关。微生物衍生物 细菌孔形成毒素，细胞外ATP和其他病原体相关分子模式触发NLRP3炎性体的激活。最近的研究报道维罗帕林活性能够诱导炎症小体活性和IL-1β的产生，其中NLRP3被K的通量调节。⁺，H ⁺和Ca ²⁺以及活性氧，自噬和内质网应激。这篇综述的目的是概述维罗帕林活性的主要发现，并特别强调它们在病毒免疫中的作用以及可能的炎症小体激活剂。