#COVIDMS – Guest post

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These are trying times. The increasing number of Covid-19 cases worldwide and the rapidly expanding hotspots around the globe are only a part of our concern; it is what we don’t know, nor fully yet understand, that scares us the most and remains the focus of research. 

We’re concerned about the brain in the context of the Covid-19 infection; the potential involvement of the brain can explain, at least in part, not only the loss of smell but also some of the clinical complications of Covid-19 infection recently described by medical colleagues in China, including symptoms of brain inflammation (encephalitis) and brain stroke and/or bleed.

Scientists quickly sequenced the Covid-19 genome (also known as SARS-CoV-2) and came to understand that it binds to and exploits a specific receptor (the angiotensin-converting enzyme 2 or ACE-2 receptor) to enter the cell, much like the SARS virus of the 2008 epidemic (SARS-CoV) did. It had been shown in the past that SARS-CoV killed brain cells in experimental mice by entering the brain via the nose and through the cells that line the roof of the nasal cavity (the olfactory epithelium)—cells which include neurones responsible for the detection of odours. Interestingly one of the symptoms of Covid-19 infection is loss of smell.

This newer SARS-CoV-2 / Covid-19 virus is similar to the older SARS-CoV, but its surface protein—which enables the virus to bind to the cell—has a higher affinity for the human ACE-2 receptor as compared to the equivalent protein of SARS-CoV.

In a recent paper, Baig and colleagues discussed the distribution of the ACE-2 receptor in the human body, the current knowledge on Covid-19’s ability to invade and live in brain cells, and propose a model for the sequential mechanism leading to cerebral involvement of the Covid-19 infection. In essence, Covid-19 could:

  1. Disseminate in the circulating blood and damage the lining of the small vessels feeding the brain (the so-called microvascular endothelium) and therefore lead to brain cell death.
  2. Spread across the porous bone located at the roof of the nose (the cribriform plate of the ethmoid bone) during the early or later phases of the infection.

In either case the Covid-19 infection can lead to cerebral involvement.

We certainly need to better understand what the chances are that Covid-19 does affect the brain in a given person, to what extent it does so, how we can treat the brain symptoms properly and – most importantly – how we can prevent it. More research and more widespread testing of Covid-19 is needed, with the hope that we can identify and administer treatment promptly and effectively.

Dr Miriam Mattoscio is a Consultant Neurologist with a special interest in MS at Queen’s Hospital (Barking Havering and Redbridge University Hospitals Trust) and an Honorary Senior Clinical Lecturer at Imperial College London. She received her medical degree from G.D’Annunzio University (Chieti, Italy) then completing her neurology training and graduating Magna Cum Laude. During the last year of her specialty training she completed a visiting research program conducting a pilot clinical study in the field of Neuroimmunology at Imperial College London. She obtained a PhD in Clinical Neuroimmunology from Imperial College London, with her research on MS immunology and biology of Haematopoietic Stem Cells in MS supported by the Italian MS Society and the MRC. Miriam now leads a number of clinical research studies as a Consultant Neurologist at Queen’s Hospital, also lecturing on MS Immunology to both ICL undergraduates and Master Students in Translational Neuroscience. She collaborates with several researchers at ICL, UCLH, Bart and the London, Fondazione St. Lucia in Rome and also the University of Verona, contributing to basic and translational research studies in the field of MS immunology. She is a member of the Scientific Committee of the Italian MS Foundation (FISM).

CoI Consulted for Merk Serono, Novartis, Roche and Celgene.

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