The neuroinvasive potential of SARS‐CoV2 may play a role in the respiratory failure of COVID‐19 patients
Open accessAbstract
Following the severe acute respiratory syndrome coronavirus (SARS‐CoV) and Middle East respiratory syndrome coronavirus (MERS‐CoV), another highly pathogenic coronavirus named SARS‐CoV‐2 (previously known as 2019‐nCoV) emerged in December 2019 in Wuhan, China, and rapidly spreads around the world. This virus shares highly homological sequence with SARS‐CoV, and causes acute, highly lethal pneumonia coronavirus disease 2019 (COVID‐19) with clinical symptoms similar to those reported for SARS‐CoV and MERS‐CoV. The most characteristic symptom of patients with COVID‐19 is respiratory distress, and most of the patients admitted to the intensive care could not breathe spontaneously. Additionally, some patients with COVID‐19 also showed neurologic signs, such as headache, nausea, and vomiting. Increasing evidence shows that coronaviruses are not always confined to the respiratory tract and that they may also invade the central nervous system inducing neurological diseases. The infection of SARS‐CoV has been reported in the brains from both patients and experimental animals, where the brainstem was heavily infected. Furthermore, some coronaviruses have been demonstrated able to spread via a synapse‐connected route to the medullary cardiorespiratory center from the mechanoreceptors and chemoreceptors in the lung and lower respiratory airways. Considering the high similarity between SARS‐CoV and SARS‐CoV2, it remains to make clear whether the potential invasion of SARS‐CoV2 is partially responsible for the acute respiratory failure of patients with COVID‐19. Awareness of this may have a guiding significance for the prevention and treatment of the SARS‐CoV‐2‐induced respiratory failure.
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Evidence of CNS invasion through neuronal retrograde routes was reported for coronaviruses HCoV-OC43, HEV67 and avian bronchitis virus.
“Evidence of CNS invasion through neuronal retrograde routes was reported for coronaviruses, such as HCoV-OC43, HEV67 and avian bronchitis virus [32].”
From Hyperactivation of P2X7 receptors as a culprit of COVID-19 neuropathology (2021) · cites this paper as [32]
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- Authors
- Li, Y., Bai, W., & Hashikawa, T.
- Affiliations
- Department of Histology and Embryology, College of Basic Medical Sciences, Norman Bethune College of Medicine Jilin University Changchun Jilin China
- Institute of Acupuncture and Moxibustion China Academy of Chinese Medical Science Beijing China
- RIKEN (JP)
- ORCID
- Li, Yan‐Chao
- Venue
- Journal of Medical Virology
- Publisher
- Wiley
- Published
- 2020-03-11
- Volume
- 92
- Issue
- 6
- Pages
- 552-555
- ISSN
- 0146-6615 (ISSN-L)
- 1096-9071
- PMC
- PMC7228394
- OpenAlex
- W3007201727
- Cited by
- 2,266
- References
- 54
- Citations by year
- 2026: 10 · 2025: 38 · 2024: 84 · 2023: 150 · 2022: 315 · 2021: 633 · 2020: 1033 · 2019: 1
- FWCI
- 59.82
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Medical Virology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Neurology › Long-Term Effects of COVID-19
- Health Sciences › Medicine › Infectious Diseases › SARS-CoV-2 and COVID-19 Research
- Health Sciences › Medicine › Infectious Diseases › COVID-19 Clinical Research Studies
- Keywords
- SARS-CoV-2, COVID-19 pandemic, neuroinvasion, central nervous system infection, acute respiratory failure, neurological symptoms, brainstem infection, respiratory distress, intensive care
- MeSH terms
- Betacoronavirus, COVID-19, SARS-CoV-2, Central Nervous System, China, Headache, Humans, Lung, Nausea, Pneumonia, Viral, Respiratory Insufficiency, Vomiting, Coronavirus Infections, Mechanotransduction, Cellular, Severe Acute Respiratory Syndrome, Severe acute respiratory syndrome-related coronavirus, Pandemics
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