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Differential interferon gene expression in bronchiolitis caused by respiratory syncytial virus-A genotype ON1.

呼吸道合胞病毒-A基因型on1 引起的毛细支气管炎干扰素基因表达差异。

  • 影响因子:3.05
  • DOI:10.1007/s00430-019-00633-6
  • 作者列表:"Pierangeli A","Viscido A","Bitossi C","Frasca F","Gentile M","Oliveto G","Frassanito A","Nenna R","Midulla F","Scagnolari C
  • 发表时间:2020-02-01
Abstract

:Bronchiolitis severity is determined by a complex interaction among viral replication and antiviral immunity. The current respiratory syncytial virus (RSV)-A, genotype ON1 demonstrated a high replicative capacity but seemed to be clinically less severe than the previously circulating RSV-A, NA1. To learn insights about ON1 innate immune response, we analyzed expression levels of type I/III interferon (IFN)-related genes in the respiratory mucosa of infants with RSV bronchiolitis. We enrolled RSV-positive bronchiolitis patients over 12 epidemic seasons at a university hospital in Rome. From nasopharyngeal washings' cells (46 positive to NA1, 47 to ON1 and 28 to RSV-B, genotype BA), the mRNA copy number of the type III IFN receptor (IFNLR1 and IL10RB subunits), and of the type I/III IFN-stimulated genes, MxA and ISG56, was calculated using the threshold cycle relative quantification method with respect to an invariant gene. Expression levels of type III IFN receptor subunits genes positively correlated to each other and did not differ in infants infected with different RSV genotypes. The ISGs levels also positively correlated between them but differed among groups. MxA levels were significantly higher in NA1-infected infants than in those with ON1 and BA; ISG56 expression was slightly higher in NA1 than in the other strains. Interestingly, a moderate negative correlation existed between viral load and both ISGs values in ON1-infected infants only. The reduced ISG levels elicited during infections with ON1 (and BA) may cause a weaker control of RSV replication and/or an inadequate host immune response which may impact the risk of respiratory sequelae.

摘要

: 毛细支气管炎的严重程度是由病毒复制和抗病毒免疫之间复杂的相互作用决定的。目前的呼吸道合胞病毒 (RSV)-A基因型ON1 表现出较高的复制能力,但在临床上似乎不如以前循环的RSV-a,na1 严重。为了了解ON1 固有免疫应答的见解,我们分析了RSV毛细支气管炎婴儿呼吸道黏膜中I/III型干扰素 (IFN) 相关基因的表达水平。我们在罗马一所大学医院招募了超过 12 个流行季节的RSV阳性毛细支气管炎患者。从鼻咽冲洗液细胞 (NA1 阳性 46 例,ON1 阳性 47 例,RSV-B阳性 28 例,基因型BA),III型IFN受体 (IFNLR1 和IL10RB亚单位) 的mRNA拷贝数,以及I/III型IFN刺激基因,MxA和ISG56,使用关于不变基因的阈值周期相对定量方法计算。Ⅲ 型IFN受体亚基基因的表达水平相互正相关,在不同RSV基因型感染的婴儿中没有差异。ISGs水平在它们之间也呈正相关,但在组间存在差异。MxA水平在NA1-infected婴儿中显著高于ON1 和BA; ISG56 在NA1 中的表达略高于其他菌株。有趣的是,病毒载量和两个ISGs值之间存在中度负相关,仅ON1-infected婴儿。感染ON1 (和BA) 时引起的ISG水平降低可能导致RSV复制控制较弱和/或宿主免疫反应不足,这可能影响呼吸系统后遗症的风险。

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呼吸道感染方向

呼吸道感染分为上呼吸道感染与下呼吸道感染。上呼吸道感染是指自鼻腔至喉部之间的急性炎症的总称,是最常见的感染性疾病。下呼吸道感染是最常见的感染性疾患,治疗时必须明确引起感染的病原体以选择有效的抗生素。

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