School of Systems Biology, George Mason University, Fairfax, Virginia (N.K.) and Schar School of Policy and Government, George Mason University, Arlington, Virginia (J.L.O.)
School of Systems Biology, George Mason University, Fairfax, Virginia (N.K.) and Schar School of Policy and Government, George Mason University, Arlington, Virginia (J.L.O.).
Mol Pharmacol. 2020 May;97(5):351-353. doi: 10.1124/molpharm.120.000014. Epub 2020 Apr 1.
COVID19 is a devastating global pandemic with epicenters in China, Italy, Spain, and now the United States. While the majority of infected cases appear mild, in some cases, individuals present serious cardiorespiratory complications with possible long-term lung damage. Infected individuals report a range of symptoms from headaches to shortness of breath to taste and smell loss. To that end, less is known about how the virus may impact different organ systems. The SARS-CoV2 virus, which is responsible for COVID19, is highly similar to SARS-CoV. Both viruses have evolved an ability to enter host cells through direct interaction with the angiotensin converting enzyme (ACE) 2 protein at the surface of many cells. Published findings indicate that SARS-CoV can enter the human nervous system with evidence from both postmortem brains and detection in cerebrospinal fluid of infected individuals. Here, we consider the ability of SARS-CoV2 to enter and infect the human nervous system based on the strong expression of the ACE2 target throughout the brain. Moreover, we predict that nicotine exposure through various kinds of smoking (cigarettes, electronic cigarettes, or vape) can increase the risk for COVID19 neuroinfection based on known functional interactions between the nicotinic receptor and ACE2. We advocate for higher surveillance and analysis of neurocomplications in infected cases. SIGNIFICANCE STATEMENT: The COVID19 epidemic has spurred a global public health crisis. While many of the cases requiring hospitalization and intensive medical care center on cardiorespiratory treatment, a growing number of cases present neurological symptoms. Viral entry into the brain now appears a strong possibility with deleterious consequences and an urgent need for addressing.
COVID19 是一场毁灭性的全球大流行疫情,中国、意大利、西班牙和现在的美国是疫情中心。虽然大多数感染病例表现为轻度,但在某些情况下,个体出现严重的心肺并发症,可能导致长期肺部损伤。受感染的个体报告了一系列症状,从头痛到呼吸急促,再到味觉和嗅觉丧失。为此,人们对病毒如何影响不同的器官系统知之甚少。导致 COVID19 的 SARS-CoV2 病毒与 SARS-CoV 非常相似。这两种病毒都进化出了通过与许多细胞表面的血管紧张素转化酶(ACE)2 蛋白直接相互作用进入宿主细胞的能力。已发表的研究结果表明,SARS-CoV 可以进入人类神经系统,这一点既有来自感染个体死后大脑的证据,也有来自脑脊液检测的证据。在这里,我们根据 ACE2 靶标在整个大脑中的强烈表达,考虑 SARS-CoV2 进入和感染人类神经系统的能力。此外,我们预测,由于尼古丁受体和 ACE2 之间已知的功能相互作用,通过各种吸烟(香烟、电子烟或蒸气烟)暴露于尼古丁会增加 COVID19 神经感染的风险。我们提倡对感染病例中的神经并发症进行更高的监测和分析。意义:COVID19 疫情引发了全球公共卫生危机。虽然许多需要住院和重症医疗护理的病例都集中在心肺治疗上,但越来越多的病例出现了神经系统症状。病毒进入大脑的可能性现在很大,可能会产生有害后果,急需解决。