Abstract

As the pandemic of COVID-19 is raging around the world, the mysteriousness of severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2) coronavirus is being revealed by the concerted endeavors of scientists. Although fever and pneumonia are typical symptoms, COVID-19 patients exhibit multiple neurological complications. In this interim review, we will summarize the neurological manifestations and their potential causes in COVID-19. Similar to the other two fatal respiratory coronaviruses, SARS-CoV and Middle East respiratory syndrome coronavirus (MERS-CoV), SARS-CoV-2 also shows to be neuroinvasive that may spread from the periphery to brain, probably by the retrograde axonal transport. The invaded viruses may directly disrupt the complex neural circuits, and raise a chronic activation of immune responses. In another hand, multiple organ failure in severe COVID-19 is caused by the systemic acute immune responses, and unsurprisingly caused the brain inflammation and led to encephalitis. However, in the central nervous system (CNS), the activation of resident immune cells including microglia and astrocytes may lead to chronic immune imbalance, which underlies the potential long-term effects in synaptic changes and neuropsychiatric impairments. The neuroinvasive biology also provides a possible link with the Braak staging of neurodegenerative diseases such as Parkinson's disease (PD). Although with considerable advances, the neurotropic potential and chronic neurological effects caused by SARS-CoV-2 infections merit further investigations.

Highlights

  • The ongoing spread of COVID-19 disease, is the first pandemic ever caused by coronaviruses in the human history, as announced by the World Health Organization (WHO) in March 2020

  • As we are in Neurological Insight Into COVID-19 the midst of this ongoing pandemic, it has gathered the concerted efforts of clinicians, public health experts, virologists, immunologists, and other scientists to understand the virus’s biology and blocking agents

  • The typical symptoms of COVID-19, unsurprisingly, are fever, cough, and pneumonia, which probably lead to acute respiratory distress syndrome (ARDS) and acute lung injury, as described in around 20% of COVID-19 patients [8]

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Summary

INTRODUCTION

The ongoing spread of COVID-19 disease, is the first pandemic ever caused by coronaviruses in the human history, as announced by the World Health Organization (WHO) in March 2020. SARS-CoV-2 is a single-stranded RNA virus, whose genome contains 29,891 nucleotides in size and 12 putative functional open reading frames (ORFs) [1] Of those translated proteins, the spike proteins located on the virus surface mediate the virus entry into host cells [2, 3]. The spike of SARS-CoV-2 senses the angiotensin converting enzyme 2 (ACE2) receptor [2,3,4,5], the same as SARS-CoV, which normally helps regulate blood pressure and anti-atherosclerosis [6] This binding, in concert with host proteases, principally TMPRSS2, facilitates the virus getting through the cell membrane by endocytosis [4], followed by hijacking the host cell’s translation machinery and producing massive virus copies and further invading new cells. The similarity goes to the systemic organ injury and cytokine storm in severe situations

SYSTEMIC ORGAN INJURY
NEUROLOGICAL MANIFESTATIONS
CYTOKINE STORM
CNS IMMUNE RESPONSES
Findings
LINKING WITH NEURODEGENERATIVE DISEASES
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