靶向病毒ORF3a蛋白:减轻COVID-19诱导的免疫细胞凋亡和相关呼吸道并发症的新方法

IF 3.1 Q2 PHARMACOLOGY & PHARMACY Advanced pharmaceutical bulletin Pub Date : 2023-11-01 Epub Date: 2023-01-23 DOI:10.34172/apb.2023.069
Minu Treeza M, Sanu Augustine, Aparna Ann Mathew, S K Kanthlal, Rajitha Panonummal
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引用次数: 0

摘要

当前,新型冠状病毒感染(SARS-CoV-2)日益成为全球公众福祉关注的问题。不同的氨基酸突变改变了SARS-CoV-2的生物学和流行病学特征以及免疫抗性。病毒引起的肺功能损害和炎症细胞因子风暴与其临床表现直接相关。但是,炎症反应的基本机制被发现是免疫细胞死亡的原因,导致宿主免疫系统功能衰竭。免疫细胞的凋亡是病毒诱导的程序性细胞死亡的最常见形式之一,因为它具有生存和毒力特性。ORF3a是一种SARS-CoV-2附属病毒蛋白,可诱导宿主细胞凋亡并抑制防御机制。这表明抑制SARS-CoV-2 ORF3a蛋白通过促进宿主免疫防御机制是治疗COVID-19感染的良好治疗策略
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Targeting Viral ORF3a Protein: A New Approach to Mitigate COVID-19 Induced Immune Cell Apoptosis and Associated Respiratory Complications.

Infection with SARS-CoV-2 is a growing concern to the global well-being of the public at present. Different amino acid mutations alter the biological and epidemiological characteristics, as well as immune resistance of SARS-CoV-2. The virus-induced pulmonary impairment and inflammatory cytokine storm are directly related to its clinical manifestations. But, the fundamental mechanisms of inflammatory responses are found to be the reason for the death of immune cells which render the host immune system failure. Apoptosis of immune cells is one of the most common forms of programmed cell death induced by the virus for its survival and virulence property. ORF3a, a SARS-CoV-2 accessory viral protein, induces apoptosis in host cells and suppress the defense mechanism. This suggests, inhibiting SARS-CoV-2 ORF3a protein is a good therapeutic strategy for the treatment in COVID-19 infection by promoting the host immune defense mechanism.

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来源期刊
Advanced pharmaceutical bulletin
Advanced pharmaceutical bulletin PHARMACOLOGY & PHARMACY-
CiteScore
6.80
自引率
2.80%
发文量
51
审稿时长
12 weeks
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