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肺移植患者的SARS-CoV-2遗传突变的动态多样性,患者患有持续的COVID-19

Hidetoshi Igari^1,2,3,4, Seiichiro Sakao^5,6, Takayuki Ishige⁷

¹Department of Infectious Diseases, Chiba University Hospital, Chiba, Chiba, Japan. igari_h@chiba-u.jp.

Nature communications

|April 29, 2024

概括

在免疫抑制患者中,SARS-CoV-2的治疗不充分可能导致耐药变种. 这一案例突显了Omicron BA.5中的突变,包括nsp12中的C799F,赋予了remdesivir耐药性.

科学领域:

病毒学病毒学
免疫学免疫学免疫学
遗传学遗传学是一个

背景情况:

严重急性呼吸系统综合征冠状病毒2 (SARS-CoV-2) 变种对COVID-19治疗构成挑战.
雷梅西维尔 (RDV) 是一种抗病毒药物,但其有效性在免疫抑制个体中可能是有限的.
在接受RDV.治疗的免疫功能低下患者中,可能会发生持续性感染和病毒泄漏.

研究的目的:

在免疫抑制肺移植接受者中描述SARS-CoV-2 Omicron BA.5感染的临床病例.
调查在RDV治疗期间出现病毒突变和耐药性的情况.
为了确定赋予对remdesivir耐药性的特定突变.

主要方法:

全基因组测序用于分析病毒种群和突变.
在移植后的患者中分析病毒分泌和融合性.
鉴定与治疗失败相关的病毒RNA依赖RNA聚合酶 (RdRp) 中的突变.

主要成果:

这位患者是一名免疫抑制肺移植接受者,经历了持续的SARS-CoV-2 Omicron BA.5感染,并患有慢性病毒泄漏.
RDV治疗导致了各种SARS-CoV-2突变的出现.
鉴定出一种特定的突变,nsp12中的C799F,通过阻止其活性形式与病毒RdRp结合,从而赋予对remdesivir的耐药性.

结论:

在免疫抑制宿主中治疗不充分可以推动SARS-CoV-2的演变成为耐药变体.
在nsp12中的C799F突变是抗雷梅西维尔耐药性的关键机制.
持续监测病毒突变对于管理持续的SARS-CoV-2感染至关重要,特别是在脆弱人群中.

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