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通过阻断病毒诱导的化,预防人类流感和冠状病毒单一或共感染
Md Ruhul Amin1, Khandaker N Anwar1, M J Ashraf2
1Division of Infectious Diseases, Department of Medicine, University of Illinois Chicago, Illinois, USA.
Antiviral research
|November 24, 2024
概括
流感A病毒 (IAV) 和冠状病毒OC43 (HCoV-OC43) 的共感染会增加酸和酸转移酶 (ST) 的活性. 抑制STs为这些呼吸道病毒提供了广泛的抗病毒策略.
科学领域:
- 病毒学 病毒学
- 细胞生物学 细胞生物学
- 药物发现 药物发现 药物发现
背景情况:
- 甲型流感病毒 (IAV) 和特有冠状病毒 (eCoV) 导致严重的呼吸系统疾病.
- 人类H1N1和HCoV-OC43可以导致严重的结果,如ARDS和死亡,特别是在弱势群体中.
- 这些病毒利用宿主细胞酸 (Sia) 结合的受体进入,由酸转移酶 (STs) 合成.
研究的目的:
- 研究基转移酶 (STs) 在H1N1和HCoV-OC43单和共感染中的作用.
- 探索STs作为潜在的宽频抗病毒目标.
- 在相关的细胞模型中评估泛ST抑制剂的疗效和安全性.
主要方法:
- 在空气流体接口 (ALI) 开发了一种人类初级小气道上皮细胞 (HSAEC) 模型,以模拟体内条件.
- 用H1N1和HCoV-OC43注射HSAEC以建立单一和共感染模型.
- 测量了酸水平,ST表达和活性,并评估了泛ST抑制剂 (3Fax-Peracetyl Neu5Ac) 的宿主细胞毒性.
主要成果:
- H1N1和HCoV-OC43单和共感染增加了酸水平和病毒协同作用.
- 受感染的细胞表现出较高的ST表达和活性.
- 全ST抑制剂有效地阻止了ST活性,而不会引起宿主细胞毒性.
结论:
- 由STs介导的化对于H1N1和HCoV-OC43感染至关重要.
- 针对STs是一个有希望的广泛的抗病毒策略来对抗这些呼吸道病毒.
- 全ST抑制提供了一种潜在的治疗方法来对抗病毒感染,克服耐药性挑战.
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