Evidence of the COVID-19 Virus Targeting the CNS: Tissue Distribution, Host–Virus Interaction, and Proposed Neurotropic Mechanisms

By A. Baig, Areeba Khaleeq, Usman Ali, Hira Syeda. ACS Chemical Neuroscience, 2020

2,005 citations recorded by the source corpus.

The recent outbreak of coronavirus infectious disease 2019 (COVID-19) has gripped the world with apprehension and has evoked a scare of epic proportion regarding its potential to spread and infect humans worldwide. As we are in the midst of an ongoing pandemic of COVID-19, scientists are struggling to understand how it resembles and differs from the severe acute respiratory syndrome coronavirus (SARS-CoV) at the genomic and transcriptomic level. In a short time following the outbreak, it has been shown that, similar to SARS-CoV, COVID-19 virus exploits the angiotensin-converting enzyme 2 (ACE2) receptor to gain entry inside the cells. This finding raises the curiosity of investigating the expression of ACE2 in neurological tissue and determining the possible contribution of neurological tissue damage to the morbidity and mortality caused by COIVD-19. Here, we investigate the density of the expression levels of ACE2 in the CNS, the host–virus interaction and relate it to the pathogenesis and complications seen in the recent cases resulting from the COVID-19 outbreak. Also, we debate the need for a model for staging COVID-19 based on neurological tissue involvement.

Subfields: Infectious Diseases, Neurology

View Paper: https://www.semanticscholar.org/paper/e31e5667244df47cec48f95d8d433e9fb4b514a7

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Infectious Diseases

1. A. Asadi-Pooya
2. Leila Simani

In Neurology

1. A. Asadi-Pooya
2. V. Perry
3. Irene Tracey
4. Leila Simani
5. C. Cunningham
6. R. Ransohoff

Citations in the corpus

• Multidisciplinary research priorities for the COVID-19 pandemic: a call for action for mental health science (2020, background): “108,109 Alternatively, SARS-CoV-2 might invade the brain from the blood, if circulating particles of the virus were transported across the blood–brain barrier by binding to ACE2 receptors expressed by endothelial cells, 109 or if infected leucocytes could carry the virus with them as they migrate…”
• Central nervous system manifestations of COVID-19: A systematic review (2020, methodology): “Through the search strategy, we could identify two articles about neurological involvement by COVID-19 (Tables 1 and 2) [7, 8] .”
• COVID-19: angiotensin-converting enzyme 2 (ACE2) expression and tissue susceptibility to SARS-CoV-2 infection (2021, background): “[48] proposed a possible pathophysiological mechanism for the involvement of the CNS, where, via haematological dissemination or via the cribriform plate, the virus would be able to break through the blood-brain barrier and to bind to the epithelial ACE2 receptor.”
• Nervous system involvement after infection with COVID-19 and other coronaviruses (2020, background): “16 could interact with ACE2 expressed in the capillary endothelium, the virus may also damage the blood-brain barrier and enter the CNS by attacking the vascular system (Baig et al., 2020).”
• Aging in COVID-19: Vulnerability, immunity and intervention (2020, positive): “While SARS-CoV-2 has been characterized regarding its neurotrophic and neuroinvasive properties (Baig et al., 2020; Puelles et al., 2020), inflammatory cytokine release and immunopathology caused by this”
• Association of chemosensory dysfunction and COVID‐19 in patients presenting with influenza‐like symptoms (2020, result): “Early studies evaluating mechanisms of SARS-CoV2-mediated olfactory loss have suggested neurotrophic targeting of olfactory neurons versus infection of non-neural olfactory epithelial cells.(5,6) The short-lived Covid-19-related olfactory loss found in our study favors a model in which SARS-CoV2 tar”