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总体而言,COVID与菌病的关联

Gurpreet Kaur¹, Rajinder Kaur¹, Sumanpreet¹

¹Department of Human Genetics, Punjabi University, Patiala, 147002, India.

Infectious disorders drug targets

|January 22, 2024

概括

COVID-19感染引发了诸如高血糖和免疫抑制等代谢变化,增加了二次性Mucormycosis真菌感染的风险. 这些条件促进真菌生长,解释了大流行期间的爆发.

科学领域:

传染性疾病传染性疾病
菌类学菌类学是指菌类学.
病毒学病毒学
免疫学免疫学免疫学

背景情况:

由SARS-CoV-2引起的COVID-19大流行,在第二波期间,二次菌菌病感染的数量显著增加,特别是在印度.
SARS-CoV-2 感染破坏了宿主细胞受体 (例如,ACE-2,NRP-1) 和细胞代谢,导致高血糖症,糖尿病酸性脂肪酸症 (DKA),铁过载,贫血,缺氧和免疫抑制.
这些COVID-19引起的生理变化为Mucormycosis真菌的扩散创造了有利的环境.

研究的目的:

探索COVID-19和粘菌菌病之间的功能性相互依赖.
总结潜在的协同作用的联系,有助于增加COVID-19患者的粘菌菌病的发病率.

主要方法:

这是一篇综述性文章,综合了有关COVID-19和菌根病之间的相互作用的现有研究.
分析病毒进入机制及其对宿主细胞过程的影响.
检查SARS-CoV-2感染的代谢和免疫后果.

主要成果:

SARS-CoV-2 感染可提高 GRP-78 受体的调节,这是 Mucormycosis 菌类的关键入口.
与COVID-19相关的疾病,如高血糖症,高血症和酸性pH值,可以增强GRP-78的表达和真菌生长.
印度的SARS-CoV-2的Delta变种,广泛的类固醇使用和氧气治疗可能导致了Mucormycosis爆发.

结论:

由于COVID-19引起的代谢失调和免疫抑制显著增加了对Mucormycosis的易感性.
提高GRP-78的调节和创造一个有利于真菌生长的环境,解释了观察到的粘菌菌病的流行.
了解这些联系对于在病毒大流行期间管理共同感染至关重要.

关键词:

在 COVID-19 疫情中,在GRP-78中使用.糖尿病酸性脂肪酸症 (DKA)过高血糖症 (hyperglycemia) 是一种疾病.免疫抑制. 免疫抑制.铁过载是什么?铁过载是什么?粘膜性肌肉病的发生.

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