March 21 Update: how do we stop COVID-19?
- March 21, 2020
March 21, 2020
It’s a quiet Saturday morning on campus. Sometimes I wonder and hope that MDI is so far away from the epicenters of this COVID-19 epidemic that perhaps we may escape the worst. You may remember that two days ago the first infection in Hancock County was reported — today this patient has disappeared from the charts; it turns out the patient lived in Penobscot County, but was tested in Hancock.
Two frequently asked questions are: How will the epidemic stop? Will we become immune against the virus?
There are, in principle, three strategies to stop the spread of COVID-19. The first is the extreme form of “social distancing” with restrictions placed on free movement and assembly – as we are seeing in parts of Europe now. This, together with an aggressive testing strategy, could interrupt the transmission of the virus entirely. However, even in European countries where curfews and severe restrictions are in place (certain parts of Germany, Austria and France) it appears to already be too late for such an approach.
The second strategy is a vaccine against the virus. Eventually, such a vaccine will be developed (just as with the flu virus) that could potentially protect everyone. Presently, scientists believe that it will take at least a year before we have a vaccine. Right now, a small biotech in Tübingen, a small university town in the south of Germany (a bit like Ann Arbor) has the most advanced strategy (this is the one Donald Trump wanted to buy).
The third strategy is to wait until enough people have been infected and become immune against the virus. You might know this as “herd immunity”. This is the approach that was initially chosen in the UK. Boris Johnson has now done an about-face on this approach, because modeling shows that the number of people affected if you do not quarantine sick patients are staggering. This scenario may very quickly lead to hospitals and healthcare providers being overwhelmed by the numbers of sick, as has happened in Italy.
The question behind these different approaches to stop the epidemic is: How does our immune system react when we are infected with COVID-19, and can we become infected twice?
Researchers at the Doherty Institute* in Australia were able to test blood samples, taken at four different time points throughout infection and recovery, in an otherwise-healthy woman in her 40s, who presented with COVID-19 and had mild-to-moderate symptoms requiring hospital admission.
So, how did the patient’s immune system respond to the virus? The researchers observed a robust immune response across different cell types. They saw an increase in specialized helper T cells, killer T cells, and B cells. This strong immune response was associated with clinical recovery, similar to what in seen with influenza cases. Seven to nine days after the first symptoms, there was an increase in immunoglobulins — which are the most common type of antibodies — rushing to fight the virus. This increase in immunoglobulins persisted up to day 20 after symptom onset.
These findings indicate that we develop an immune response and immunity against the coronavirus. Since the virus is a “lazy” virus and does not mutate easily (much less than the flu virus) it is very likely that after an infection a person will have obtained long-term immunity and will not be infected by coronavirus again.
It is reassuring to see how our body can fight back – there is hope that we can fight the disease and remain protected.
* The patient report has been published by: Irani Thevarajan, Thi H. O. Nguyen, Marios Koutsakos, Julian Druce, Leon Caly, Carolien E. van de Sandt, Xiaoxiao Jia, Suellen Nicholson, Mike Catton, Benjamin Cowie, Steven Y. C. Tong, Sharon R. Lewin, Katherine Kedzierska. Breadth of concomitant immune responses prior to patient recovery: a case report of non-severe COVID-19. Nature Medicine, 2020.
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