Abstract
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a novel member of the genus of betacoronavirus, which caused a pandemic of coronavirus disease 2019 (COVID-19) worldwide. The innate immune system plays a critical role in eliminating the virus, which induces inflammatory cytokine and chemokine secretion, produces different interferons, and activates the adaptive immune system. Interactions between the autonomic nervous system and innate immunity release neurotransmitters or neuropeptides to balance the excess secretion of inflammatory cytokines, control the inflammation, and restore the host homeostasis. However, more neuro-immune mechanisms to defend against viral infection should be elucidated. Here, we mainly review and provide our understanding and viewpoint on the interaction between respiratory viral proteins and host cell receptors, innate immune responses to respiratory viral infection, and the autonomic neural regulation of the innate immune system to control respiratory viruses caused by lungs and airways inflammation.
Highlights
At the end of 2019, an emerging severe acute respiratory infectious disease outbreak occurred in Wuhan, China (Hu et al, 2020)
The released cytokines bind to the receptors of the neurons to activate the sympathetic nervous system (SNS) and parasympathetic nervous system (PNS) to secrete noradrenaline or acetylcholine neurotransmitters and neuropeptides, which bind to the receptors of the respiratory target cells to suppress excessive proinflammatory cytokine production and regulate physiological functions of the respiratory system to protect against viral infection (Figure 1)
This study focused on autonomic nervous system (ANS)-mediated innate immune responses to defend against SARS-CoV-2 infection
Summary
At the end of 2019, an emerging severe acute respiratory infectious disease outbreak occurred in Wuhan, China (Hu et al, 2020). Based on the current research, we discuss and explain autonomic neural regulation of the innate immune responses to SARS-CoV-2 infection through adrenergic or cholinergic pathways and neuropeptides in this study.
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