严重急性呼吸道综合征冠状病毒2和流感A病毒之间的病毒干扰
Shella Gilbert-Girard1, Jocelyne Piret1, Julie Carbonneau1
1Research Center of the CHU de Québec-Université Laval, Quebec City, Quebec, Canada.
PLoS pathogens
|July 22, 2024
概括
流感A型病毒,特别是A/H3N2,通过激活干扰素通路来干扰SARS-CoV-2的复制. SARS-CoV-2不会显著干扰流感,同时感染会降低干扰素反应,影响病毒相互作用.
科学领域:
- 病毒学 病毒学
- 免疫学 免疫学 免疫学
- 呼吸道病原体的相互作用
背景情况:
- 通过干扰素 (IFN) 途径介导的病毒干扰可以影响共感染.
- 在COVID-19流行病中,非药物干预措施限制了对SARS-CoV-2共感染的研究.
- 随着限制的放松,预计SARS-CoV-2和流感A病毒将共同传播,需要进行相互作用研究.
研究的目的:
- 为了研究SARS-CoV-2 (Omicron和祖先菌株) 和流感A病毒 (A/H3N2和A/H1N1) 之间的病毒干扰.
- 为了比较这些病毒对干扰素产生和干扰素刺激基因表达 (ISG) 的影响.
- 确定每个病毒对外源性I型和III型干扰素的敏感性.
主要方法:
- 人类呼吸道上皮的感染与SARS-CoV-2和流感A病毒,同时或顺序.
- 使用RT-qPCR量化病毒载荷.
- 测量IFN-α/β/λ蛋白和ISG表达 (OAS1/IFITM3/ISG15/MxA) 通过免疫测试和RT滴滴数字PCR.
- 对复合IFN-α/β/λ2蛋白的病毒敏感性的评估.
主要成果:
- 流感A,特别是A/H3N2,对SARS-CoV-2两种菌株都表现出显著的干扰.
- SARS-CoV-2 没有显著干扰流感 A/H3N2 或 A/H1N1.
- 与SARS-CoV-2相比,流感A/H3N2诱导了更高的IFN蛋白质生产和ISG表达.
- SARS-CoV-2 诱导了最小的 IFN 生产,并在同感染期间降低了 IFN 反应.
- 所有病毒都对外源IFN敏感;祖先的SARS-CoV-2和Omicron分别对I型和III型IFN敏感性降低.
结论:
- 流感A,特别是A/H3N2,会干扰SARS-CoV-2,可能是通过干扰素介导的机制.
- 然而,SARS-CoV-2并没有显著干扰流感A病毒.
- 同感染导致整体干扰素反应减弱,突出显示复杂的病毒相互作用.
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