#COVIDMS Immune Response of a COVID Survivor


So what is important for the immune response to COVID?

In this COVID survivor we see the kinetics of the immune response as it generates after infection. To me it is as expected. It is a combination of T and B cells and the innate (monocytes etc). immune response and occurs according to Immunology 101. B cell responses take a few days to generate and antibody producing cells are elevated by about 8 days after symptom onset, with recovery from day 10. The antibody ramps up after that, because this is what is going to do. It creates a response that is going to be rapidly produced on next encounter and is designed to stop you getting re-infected. This is what antibodies do.

I bet when the sequences of the B cell receptor are cloned and made, you will see some of them being made are to the “Spike protein” of the virus, which it uses to infect the lungs.

The T cells and notably the CD8 T cell response is there by 7 days and is highest by day 9 and is again consistent with immunology 101 that CD8 T cells are the best beasties for kicing some viral butt. There was an increase in CD4, not a mega increase and they will be doing what they do and that is help B cells to make antibody and help CD8 T cells to kill virus. Does that make them top dog. In the eyes of the MS immunologist it seems so. The Immune system is a system and uses more than one thing to get the job done, which is kill the infection.

I guess it doesn’t tell us what would happen if one of the cell types are not there, but you can see the viral load is already dropping dramatically at day 7 when the antibody level has yet to really pick up and I think it says “CD8 cavalry to the rescue” along with the innate system. They are probably not in the blood because they are in the lung doing their job.

Therefore, you may be at early risk with alemtuzumab because these cells, notably the CD8 T cell are depleted. In reallity cladribine is a magnitude less active on these cells and really does not do alot of damage to the innate immune system at the dose used in MS. Also ocrelizumab is an another order of magnitude lower at depleting CD8 T cells. Whilst it may cause a blunted antibody response…if CD8 T cells and the innate immune response at the front line in ridding people of the the COVID virus it makes one wonder if we should be lumping all IRTS together. It perhaps says that to suggest that the agents have the same risk does not seem to take into account the biology. Also this risk will change with time, because once the treatments are gone the cells come back. HSCT is going to be at top of the tree, as it depletes CD8 T cells alot and B cells alot and so much so that you have to re-do vaccinations.

However the authors put the emphasis of the antibody secreteing cells and the follicular T helper cells.

Remeber this person was not really treated and the the course was mild. There was no increase in cytokines like-interleukin 6, which ahs been associated with a worsening.

Where would you put your emphasis

Thevarajan I et al. Breadth of concomitant immune responses prior to patient recovery: a case report of non-severe COVID-19.Nature medicine (2020).


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  • Thanks for this explanation MD.
    Very striking this person had mild course and wasn’t really treated.
    My non-scientific response being – as there’s still lack of determining knowledge as to the level of risk then I’m gonna continue to happily self isolate as someone who, due to Alem, has lymphocytes below 0.8

    • Sadly not being treated is the new reality for some individuals in Italy…Keeping out of the way is the safest bet but how long can we do it for.

      • Think I may have misunderstood when reading your post because I interpreted ‘wasn’t really treated’ as someone not really requiring treatment – due to having mild symptoms.
        The situation in Italy is just too awful and repeatedly provides reason to be distressed! Reading of nearly 3000 HCPs infected and 13 doctors dead, including the two who came out of retirement to help, makes me hope so much that our NHS isn’t overwhelmed and that, like Italy, our heroes aren’t having to be not the armed forces, but those medics on the frontline!

    • Just standard of care because I am guessing their symtoms did not warrant other interventions, just Australian TLC was enough

  • What about a situation where cladribine has completely reduced monocytes? I’m aware that’s not supposed to happen and am curious what mechanism would allow this.

    • It is a dose related event, the higher doses reduce monocyctes, I guess there have been people you may do so with the oral variant, I could check this in the data we have, but am rather snowed under with student issues

      • I understand. I look forward to finding out more about this. I was concerned with the weight dosing of oral cladribine and hoped to be treated as “lighter weight” due to my history of being a super responder to medications. But with protocols, it’s not possible.

        Would love to see repopulation research on more than lymphocytes. I’m not thrilled that my innate immune system has taken a hit at this time.

  • What about Nk cell?

    They kill virus too

    And they interact with hla type 2

    “The understanding has been that NK cells interact with HLA class 1 but not class 2. The identification of a mechanism that class 2 uses to interact with NK cells changes our perception of NK cell biology,” says study co-author Paul Norman, Ph.D., CU Cancer Center investigator and associate professor in the CU School of Medicine Division of Personalized Medicine, and Department of Microbiology and Immunology.”


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