Corona virus and it’s neurotrophic potential

Before I begin writing this, I will add that I’m not an expert in this virus, or a researcher. You’ll also know that I always write disclaimers… !! As someone who has a auto immune/neurological condition, I’m always intrigued by research in these areas and this virus is no exception.

The recent outbreak of COVID-19 has gripped the world with apprehension and caused panic across all countries worldwide in epic proportions. Scientists are to some degree struggling to understand how it is similar or different to the previous corona virus infections that have come before, namely SARS and MERS.

It has already shown some similarities in that it exploits a particular receptor called Angiotensin Converting Enzyme 2 receptor (ACE 2) in order to get into our cells.

To me, this raises a few questions about whether this receptor is expressed in neurological tissues, and whether that leaves people at risk if they are taking immuno suppressants such as mine (Natalizumab) whereby there is a compartment created protecting the CNS from immune response.

What is COVID 19?

I don’t think I need to tell anyone what this virus is or when it started. I believe that everyone around the world has some level of expertise in this since we are bombarded with this on a daily basis in the varying news articles and reports on the tv. The first report of the infection was in China, in Wuhan province in December 2019. It was considered that the virus may have started in the wet meat markets, potentially coming initially from bats that were kept close to other bush meats.

I will comment that bats do not get sick from such corona viruses, and they do tend to live with them in their systems without mounting an immune response. This is curious and is thought to be due to their high level of metabolic demand. Some have considered that they may be able to look into how bats live with the virus without mounting an immune e response in order to find some answers to how we may be able to over come the infection.

Anyway – I digress. By early in February, terms such as corona virus and COVID were in use and by the 11th February, the WHO had officially named the virus. Of course the virus had been in existence long before it jumped across to be contagious in humans from animal hosts (zoonosis). Of course there in lie the problem as we have no experience in which to mount an immune response.

The ACE 2 receptor

As I mentioned before, the ACE 2 receptor is the way the virus sneaks into cells. It’s known that this receptor is in the lungs, heart, kidneys, intestines, brain, and testicles. This explains how the illness is predominantly respiratory and has been known to cause some digestive symptoms. However the central nervous system has also been known to express some of the receptors too, in glial cells and neurones which may well make them a target for COVID 19.

In previous corona outbreaks, such as the SARS outbreak, patients who died and were analysed at autopsy displayed evidence of the virus in their brain tissues, and the spinal fluid. Scientists comment on the role of the blood brain barrier in preventing the virus from accessing the CNS although there are some reports of neurological symptoms in patients.

How does the virus get into the cell?

The virus uses something called a spike protein and uses this to attach to cell membranes by the ACE 2 receptor. Interestingly, compared to the previous SARS virus, this COVID 19 is thought to have an affinity for the receptor more than 20 times higher.

How might the virus even get into the brain then?

As the viral load increases, and there is an increased amount in general circulation, it is thought that the virus may be able to pass into the cerebral circulation. When the virus moves from the capillaries, damaging the cell endothelial membrane, it is thought to favour access across the blood brain barrier. It is considered that once in this space, the virus may well interact with the ACE2 receptor on the neurones. Perhaps (although I’m speculating) this may well cause a feedback loop of viruses budding into this space, attachment and damage. I wonder if the involvement of the CNS may be the cause of the altered sense of smell in patients with COVID 19?

Why am I writing about this?

Well as someone on tysabri, i am concerned about the neurological impact of the virus. I read something the other that lead me to be more concerne that I need to make sure that I keep myself safe from this. Despite people with ms being reported to not be at an increased risk of catching the virus, and for the most part people with ms mostly reporting mild symptoms if the virus is caught, there are reportable case of meningoencephalitis with virus detectable in the spinal fluid. This means that there is an increased risk for people on natalizumab.

In fact It is so important that if you are on natalizumab and get COVID-19 that you look-out for CNS symptoms!! This was not previously reported and is a new piece of information that I’ve gleaned.

I’ve recently been shifted onto extended dosing of my tysabri. Although they haven’t recommended that I stop taking treatment as this would be more of a risk to me.. I do have my concerns. I will keep you updated as I learn more.

2 thoughts on “Corona virus and it’s neurotrophic potential

    1. Thanks John – a tough one isn’t it. The impact of the virus for people with MS seems to be a moving feast and I’m not sure I can keep up. I’m trying to keep on top of the research and read Bart’s blogs but it seems to change day to day. Hopefully people may get some use from this blog even without being concerned about the Natz aspect.


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