College of Veterinary Medicine, Henan Agricultural University, Zhengzhou, 450046, China.
Arch Virol. 2022 Feb;167(2):281-292. doi: 10.1007/s00705-021-05318-1. Epub 2021 Nov 28.
Hepatitis-hydropericardium syndrome (HHS), caused by fowl adenovirus serotype 4 (FAdV-4), has spread on chicken farms worldwide, causing huge economic losses. Currently, the exact mechanism of pathogenesis of FAdV-4 remains unknown. Despite the severe inflammatory damage observed in chickens infected with pathogenic FAdV-4, few studies have focused on the host immune system-virus interactions and cytokine secretion. Host immunity acts as one of the most robust defense mechanisms against infection by pathogens, and cytokines are important in their elimination. However, excessive inflammatory cytokine secretion could contribute to the pathogenesis of FAdV-4. Understanding of the roles of cytokines produced during FAdV-4 infection is important for the study of pathogenicity and for developing strategies to control FAdV-4. Several previous studies have addressed the immune responses to FAdV-4 infection, but there has not been a systematic review of this work. The present review provides a detailed summary of the current findings on cytokine production induced by FAdV-4 infection to accelerate our understanding of FAdV-4 pathogenesis.
肝炎-心包积水综合征（Hepatitis-hydropericardium syndrome，HHS）由禽腺病毒血清型 4（Fowl adenovirus serotype 4，FAdV-4）引起，已在全球范围内的鸡场传播，造成了巨大的经济损失。目前，FAdV-4 的确切发病机制尚不清楚。尽管感染致病性 FAdV-4 的鸡表现出严重的炎症损伤，但很少有研究关注宿主免疫系统-病毒相互作用和细胞因子分泌。宿主免疫是抵御病原体感染的最强大防御机制之一，细胞因子在其中的消除中起着重要作用。然而，过度的炎症细胞因子分泌可能导致 FAdV-4 的发病机制。了解 FAdV-4 感染过程中产生的细胞因子的作用对于研究致病性和制定控制 FAdV-4 的策略非常重要。之前的几项研究已经解决了对 FAdV-4 感染的免疫反应问题，但尚未对这项工作进行系统的综述。本综述详细总结了目前关于 FAdV-4 感染诱导细胞因子产生的研究结果，以加速我们对 FAdV-4 发病机制的理解。
