Abstract
By engaging angiotensin-converting enzyme 2 (ACE2 or Ace2), the novel pathogenic severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) invades host cells and affects many organs, including the brain. However, the distribution of ACE2 in the brain is still obscure. Here, we investigated the ACE2 expression in the brain by analyzing data from publicly available brain transcriptome databases. According to our spatial distribution analysis, ACE2 was relatively highly expressed in some brain locations, such as the choroid plexus and paraventricular nuclei of the thalamus. According to cell-type distribution analysis, nuclear expression of ACE2 was found in many neurons (both excitatory and inhibitory neurons) and some non-neuron cells (mainly astrocytes, oligodendrocytes, and endothelial cells) in the human middle temporal gyrus and posterior cingulate cortex. A few ACE2-expressing nuclei were found in a hippocampal dataset, and none were detected in the prefrontal cortex. Except for the additional high expression of Ace2 in the olfactory bulb areas for spatial distribution as well as in the pericytes and endothelial cells for cell-type distribution, the distribution of Ace2 in the mouse brain was similar to that in the human brain. Thus, our results reveal an outline of ACE2/Ace2 distribution in the human and mouse brains, which indicates that the brain infection of SARS-CoV-2 may be capable of inducing central nervous system symptoms in coronavirus disease 2019 (COVID-19) patients. Potential species differences should be considered when using mouse models to study the neurological effects of SARS-CoV-2 infection.
Highlights
Since December 2019, much attention has focused on the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and the related coronavirus disease 2019 (COVID-19) pandemic, which is rapidly spreading around the world and results in a global health emergency [1]
We mainly found: [1] the expression of ACE2 was relatively high in several specific brain areas in human; [2] the expression of ACE2 was mainly located in many neurons in the human middle temporal gyrus and posterior cingulate cortex, but it was undetectable in the human prefrontal cortex (PFC) and very low in the human hippocampus; and [3] except for the additional expression of Ace2 in the olfactory bulb areas for spatial distribution and the pericytes and endothelial cells for cell-type distribution analysis, the main distribution map of Ace2 in the mouse brain was similar to that in human
Our results revealed an outline of ACE2 or Ace2 distribution in the human and mouse brains, which supports the hypothesis that SARS-CoV-2 is capable to infect the brain and lead to central nervous system (CNS) symptoms in COVID-19 patients [36]
Summary
Since December 2019, much attention has focused on the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and the related coronavirus disease 2019 (COVID-19) pandemic, which is rapidly spreading around the world and results in a global health emergency [1]. According to a recent retrospective case series study, 53 out of 214 (24.8%) COVID-19 patients had CNS symptoms, including dizziness, headache, impaired consciousness, acute cerebrovascular disease, ataxia, and epilepsy [3]. It has been found that SARS-CoV, a previously reported similar coronavirus, spreads into the brain after it was cleared from the lung in mice, which could be more concealment than that in the lung [4]. Puelles et al found that SARS-CoV-2 has an organotropism beyond the respiratory tract, including the kidneys, liver, heart, and brain [5]. It is necessary and urgent to study the CNS infection of SARS-CoV-2
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