Department of Biochemistry, All India Institute of Medical Sciences (AIIMS), New Delhi, India; Department of Biochemistry, All India Institute of Medical Sciences (AIIMS), Rishikesh, India.
Department of Biochemistry, All India Institute of Medical Sciences (AIIMS), Rishikesh, India.
Virus Res. 2021 Jan 15;292:198235. doi: 10.1016/j.virusres.2020.198235. Epub 2020 Nov 21.
The first incidence of COVID-19 was reported in the Wuhan city of Hubei province in China in late December 2019. Because of failure in timely closing of borders of the affected region, COVID-19 spread across like a wildfire through air travel initiating a pandemic. It is a serious lower respiratory track viral infection caused by highly contagious, severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). Coronavirus including COVID-19 causing SARS-CoV-2 causes zoonotic diseases and thought to be originated from bats. Since its first incidence, the virus has spread all across the world, causing serious human casualties, economic losses, and disrupting global supply chains. As with SARS-CoV, COVID-19 causing SARS-CoV-2 follows a similar path of airborne infection, but is less lethal and more infectious than SARS and MERS. This review focusses on the pathogenesis of SARS-CoV-2, especially on the dysfunctional immune responses following a cytokine storm in severely affected persons. The mode of entry of SARS-CoV-2 is via the angiotensin converting enzyme 2 (ACE-2) receptors present on the epithelial lining of lungs, gastrointestinal tract, and mucus membranes. Older persons with weaker immune system and associated co-morbidities are more vulnerable to have dysfunctional immune responses, as most of them concomitantly have severe hypovitaminosis D. Consequently, causing severe damage to key organs of the body including lungs and the cardiovascular system. Since, vast majority of persons enters to the intensive care units and died, had severe vitamin D deficiency, thus, this area must be investigated seriously. In addition, this article assesses the role of vitamin D in reducing the risk of COVID-19. Vitamin D is a key regulator of the renin-angiotensin system that is exploited by SARS-CoV-2 for entry into the host cells. Further, vitamin D modulates multiple mechanisms of the immune system to contain the virus that includes dampening the entry and replication of SARS-CoV-2, reduces concentration of pro-inflammatory cytokines and increases levels of anti-inflammatory cytokines, enhances the production of natural antimicrobial peptide and activates defensive cells such as macrophages that could destroy SARS-CoV-2. Thus, this article provides the urgency of needed evidences through large population based randomized controlled trials and ecological studies to evaluate the potential role of vitamin D in COVID-19.
2019 年 12 月，中国湖北省武汉市首次报告了 COVID-19 病例。由于受影响地区边境未能及时关闭，COVID-19 通过航空旅行像野火一样蔓延，引发了大流行。它是一种由高度传染性的严重急性呼吸系统综合征冠状病毒 2（SARS-CoV-2）引起的严重下呼吸道病毒感染。包括 COVID-19 在内的冠状病毒引起的 SARS-CoV-2 导致人畜共患病，据认为源自蝙蝠。自首次发病以来，该病毒已在全球范围内传播，造成严重的人员伤亡、经济损失，并扰乱了全球供应链。与 SARS-CoV 一样，COVID-19 引起的 SARS-CoV-2 遵循类似的空气传播感染途径，但比 SARS 和 MERS 更具传染性和致命性。本综述重点介绍了 SARS-CoV-2 的发病机制，特别是在严重感染者中细胞因子风暴后功能失调的免疫反应。SARS-CoV-2 的进入模式是通过存在于肺部、胃肠道和黏膜上皮衬里的血管紧张素转换酶 2（ACE-2）受体。免疫系统较弱且伴有合并症的老年人更容易出现功能失调的免疫反应，因为他们大多数同时患有严重的维生素 D 缺乏症。因此，会对身体的关键器官造成严重损害，包括肺部和心血管系统。由于绝大多数人进入重症监护病房并死亡，严重缺乏维生素 D，因此必须认真研究这一领域。此外，本文评估了维生素 D 降低 COVID-19 风险的作用。维生素 D 是肾素-血管紧张素系统的关键调节剂，SARS-CoV-2 利用该系统进入宿主细胞。此外，维生素 D 调节免疫系统的多种机制来抑制病毒，包括抑制 SARS-CoV-2 的进入和复制、降低促炎细胞因子的浓度并增加抗炎细胞因子的水平、增强天然抗菌肽的产生并激活防御细胞，如巨噬细胞，可以摧毁 SARS-CoV-2。因此，本文通过大型人群随机对照试验和生态研究提供了急需的证据，以评估维生素 D 在 COVID-19 中的潜在作用。
