由SARS-CoV-2感染引起的发性心肌炎没有严重的肺部参与:对COVID-19病变发生的洞察力
Han Du1, Zhongtao Du2, Liang Wang3
1College of Life Science and Technology, Xinjiang University, Urumchi, Xinjiang 830046, China; CAS Key Laboratory of Pathogen Microbiology and Immunology, Institute of Microbiology, Center for Influenza Research and Early-warning (CASCIRE), CAS-TWAS Center of Excellence for Emerging Infectious Diseases (CEEID), Chinese Academy of Sciences, Beijing 100101, China.
严重急性呼吸道综合征冠状病毒2 (SARS-CoV-2) 可以直接感染心肌,导致 fulminant心肌炎. 在心脏和肠道中发现的独特病毒菌株表明独特的感染途径独立于肺损伤.
科学领域:
- 病毒学 病毒学
- 心脏病学 心脏病学
- 病理学 病理学 病理学
背景情况:
- 严重急性呼吸系统综合征冠状病毒2 (SARS-CoV-2) 感染与肺部和心血管并发症有关.
- 据报道,肌心炎和心力衰竭是SARS-CoV-2感染的后果.
研究的目的:
- 在发性心肌炎病例中调查SARS-CoV-2感染.
- 为了确定SARS-CoV-2是否直接感染心肌.
- 分析不同组织中的病毒遗传多样性.
主要方法:
- 两名患有SARS-CoV-2诱导的发性心肌炎的患者的案例研究.
- 心脏生物标志物分析和成像检查.
- 病毒抗原的免疫组合化学染色.
- 整个病毒基因组的下一代测序.
- 来自呼吸道,门和心肌样本的病毒菌株的遗传学分析.
主要成果:
- 患者表现为心脏生物标志物升高和肺损伤最小.
- 免疫组织化学证实了心肌细胞内的SARS-CoV-2抗原.
- 遗传学分析显示,在心肌/门样本和呼吸道样本中,有明显的病毒群.
- 在心肌/门菌株中发现了独特的突变,表明组织特异性适应.
- 在心肌组织中发现有遗传特异性SARS-CoV-2变异的证据.
结论:
- SARS-CoV-2 可以直接感染心肌,导致发性心肌炎.
- 由SARS-CoV-2引起的心肌梗塞感染可能独立于严重的肺部感染.
- 建议使用不同的病毒菌株和潜在的替代感染途径 (例如通过肠道).
- 这些发现强调了SARS-CoV-2系统性传播的潜力以及多器官评估的必要性.
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