The hypothesis that immunosuppression may protect you from severe COVID-19 is gaining traction. New data released on the 4th April 2020 from the UK’s Intensive Care National Audit & Research Centre suggests it may. When comparing 2249 patients admitted to ITU in the UK with severe COVID-19 the proportion of immunocompromised patients was 3.7x lower than the proportion of immunocompromised patients admitted to ITU with viral pneumonia (the comparator) between 2017 and 2019 (2.3% vs. 8.5%). This was a highly significant difference (p<0.00001).
This clearly justifies the current research strategy being tested across the planet to see if immunosuppressive therapies may improve disease outcome in patients with COVID-19.
Does this mean we can now assume that immunosuppression protects against severe COVID-19 and COVID-19-related ARDS (adult respiratory distress syndrome)? Not yet. The UK’s ITU cohort of severe COVID-19 is biased in that those patients who are deemed too frail and/or disabled may never get to ITU, which may include a disproportionate number of immunosuppressed patients. Whereas this specific bias is unlikely to apply to ITU admissions between 2017 and 2019 (viral pneumonia cohort) when there was no such pressure on resources.
Despite this caveat, this is an important tidbit of information that will allow pwMS on immunosuppression to sleep a bit easier. I sincerely hope the wider MS community will reconsider their advice about not giving MS DMTs that are if anything mildly immunosuppressive to patients with active MS. By not treating our patients we may unintentionally be increasing their chances of developing severe COVID-19. Could our guidelines be another example of the law of unintended consequences? Let’s hope the real-world data that is being collected at present will answer this question.
CoI: multiple
This doesn’t make sense. If a weakened immune system were protective, wouldn’t you expect young people to succumb to the virus more than old, as they did in the 1918 flu?
The data is what it is. Older people are more susceptible to flu mortality as well. In 1918-1920 we didn’t have modern medicine so you can really extrapolate from that epidemic. In addition, previous flu exposure (older people) can protect one from new strains, which may compound the results.
Fair enough. I had just always read that the cytokine storm made the 1918 flu more lethal to young healthies. I’ve heard a couple of online doctors now speculate that the cytokine storm causes COVID-19 patients to crash–which is consistent with immunosuppression being protective, but not with older people being more at risk.
It will be interesting to see how this plays out. Meanwhile, I’m totally re-upping my Ocrevus in September. Thanks for the post!
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This is the most reassuring thing ive read, to date. Thank you so much.
Could it be that the immunosuppressed are taking more extreme action in protecting themselves against Covid-19 than they do against viral pneumonia? And that is the reason for the drop in hospital admissions?
Possibly, but these cases really represent the beginning of the curve before social distancing etc. was being implemented.
This data is very biased, but at least the data goes in the right direction and supports what we are seeing with the first 200+ patients with MS who have had COVID.
Would having had two rounds of alemtuzamab in 2013 and 14 with with a lymphocyte count of 1.1 mean that I’m suppressed enough still to benefit or not?
Does this apply equally to all DMTs like the beta interferons, Gilyena, DMF, etc… equally?
No. There is a spectrum for the essentially non-immunosuppressives like beta interferons and copaxone at one end to the highly effective but initially highly immunosuppressant therapies like alemtuzumab and HSCT.
Why is Pharma investigating the beta interferons then as a TREATMENT for Corvid19?
The interferons were originally described and identified as anti-viral agents, way back when.
What about immunomodulators like Tecfidera? Your opinion?
Tecfidera can in some cases produce a low white cell count, which should be picked up by monitoring.
How does that compare with the gender ratio in the icu as women tend to have ms more often?
PLEASE look at my comments in “COVID-19 Education” about a viral hypothesis for MS 2.0: “A virus would target oligodendrocytes and not the immune system. This virus would turn the perfectly healthy immune system against the nervous system.’
This explain why immunosuppression ~work. You maim the immune system who is less capable of killing the infected oligodendrocytes.
Really important early data.
While it’s certainly possible that immunosuppressed patients may have a theoretically higher risk of contracting Covid19, this data is in line with my current thinking.
Immunosuppression may be “better”, than immunocompetence and the likely reason is that these patients are experiencing less cytokine release syndrome.
It’s why fingolimod is being studied in patients infected with Covid19.
It’s also why tocilizumab is being studied (already FDA approved for cytokine release syndrome)
I’m cautiously optimistic….
And Ruxolitinib, a JAK inhibitor also about to be studied in a clinical trial.
Ruxolitinib, a JAK inhibitor also about to be studied in a clinical trial.
Yes, I think the same. A hyperactivated immune system might be beneficial not to get infected, but if the disease is contracted, once this cytokine storm starts, it might get actually worse, hence immunosuppressed people would have higher chances to get sick, but they would (almost) never develop severe symptoms, because this cytokine storm is less likely to happen (or is less important) in their immunosuppressed background.
The virus (SARS-CoV-2) that causes disease (COVID-19) does not directly kill cells (non-cytolytic). It causes minimal direct lung tissue damage.
This is similar to other related Coronoviruses (SARS and MERS). In the vast majority of patients the virus is effectively cleared about 10 days after symptoms start.
Mortality in COVID19 patients is mediated by acute respiratory distress syndrome (ARDS) and Cytokine Release Syndrome (CRS). This is caused by a hyper-activated immune response even if the virus is cleared. This is why many clinical centres are using immune modulators (Tocilizumab & JAK inhibitors) as rescue therapies in ARDS and CRS. They are often used in combination with anti-viral therapies.
It is completely plausible that people taking immune modulators are therefore at lower risk of developing RDS & CRS. This was also clear from the early SARS and MERS evidence.
COVID-19 mortality does appear higher in older individuals and those with underlying diseases. This may be related to natural immune dysregulation associated with an ageing immune system. The data is less clear at this time.
Does immunosuppression protect you from gunshot wounds? Immunosuppressed people make up a much smaller percentage of hospitalizations from gunshot wounds than they do hospitalizations from viral pneumonia.
Hi Prof G,
Thanks for sharing this interesting data. Is the thought here that if you contract COVID-19, you may have less severe outcomes if you are immunocompromised? If so, in terms of confirming whether immunosuppression is protecting against severe COVID-19, would it be worth looking at the total number of confirmed cases of coronavirus in this population and then assessing their outcomes and comparing that same situation in non-immunocompromised individuals? A breakdown of asymptomatic, mild symptoms and severe outcomes in each cohort may give a clearer representation. Interested to hear your thoughts and if you have enough data yet to be able to achieve that.
I have been having the same thought and googling to find someone who supports my thinking. Good to see that I’m not alone