Mehboob Riffat, Kurdi Maher, Bamaga Ahmed, Aldardeir Njoud, Nasief Hisham, Moshref Leena H, Alsinani Taghreed, Rayes Almotasimbellah O, Jabbad Reem H
Faculty of Allied Health Sciences, The University of Lahore, Lahore, Pakistan.
Lahore Medical Research Center, LLP, Lahore, Pakistan.
Front Med (Lausanne). 2021 Nov 18;8:727593. doi: 10.3389/fmed.2021.727593. eCollection 2021.
Novel Severe Acute Respiratory Syndrome-Corona Virus-2 infection (SARS-CoV-2) is an acute respiratory and infectious disease. This perspective aims to provide a basic understanding of the inflammation caused by SARS-CoV-2 and its relation to the trigeminal ganglion (TG). The virus enters through the mucous membranes of the orofacial region and reaches the TG, where it resides and takes control of its peptides including Substance P (SP). SP is the main neuropeptide, neuromodulator, and neuro-hormone of TG, associated with nociception and inflammation under noxious stimulus. SP release is triggered and, consequently, affects the immune cells and blood vessels to release the mediators for inflammation. Hence, cytokine storm is initiated and causes respiratory distress, bronchoconstriction, and death in complicated cases. Neurokinin-1 Receptor (NK-1R) is the receptor for SP and its antagonists, along with glucocorticoids, may be used to alleviate the symptoms and treat this infection by blocking this nociceptive pathway. SP seems to be the main culprit involved in the triggering of inflammatory pathways in SARS-CoV-2 infection. It may have a direct association with cardio-respiratory rhythm, sleep-wake cycle, nociception, and ventilatory responses and regulates many important physiological and pathological functions. Its over-secretion should be blocked by NK-1R antagonist. However, experimental work leading to clinical trials are mandatory for further confirmation. Here, it is further proposed that there is a possibility of latency in SARS-CoV-2 virus infection if it is acting through TG, which is the main site for other viruses that become latent.
新型严重急性呼吸综合征冠状病毒2感染（SARS-CoV-2）是一种急性呼吸道传染病。本文旨在对SARS-CoV-2引起的炎症及其与三叉神经节（TG）的关系提供基本认识。病毒通过口面部区域的粘膜进入并到达TG，在那里它驻留并控制其包括P物质（SP）在内的肽。SP是TG的主要神经肽、神经调质和神经激素，在有害刺激下与伤害感受和炎症相关。SP的释放被触发，进而影响免疫细胞和血管释放炎症介质。因此，细胞因子风暴被启动，并在复杂病例中导致呼吸窘迫、支气管收缩和死亡。神经激肽-1受体（NK-1R）是SP的受体，其拮抗剂与糖皮质激素一起，可通过阻断这条伤害感受途径来减轻症状并治疗这种感染。SP似乎是SARS-CoV-2感染中触发炎症途径的主要罪魁祸首。它可能与心肺节律、睡眠-觉醒周期、伤害感受和通气反应直接相关，并调节许多重要的生理和病理功能。其过度分泌应被NK-1R拮抗剂阻断。然而，需要进行导致临床试验的实验工作以进一步证实。在此，进一步提出，如果SARS-CoV-2病毒通过TG起作用，那么它有可能存在潜伏感染，TG是其他病毒潜伏的主要部位。
