#MSCOVID19…Natural infection shows CD20 depletion reduces antibody response but what is the issue with fingolimod? I don’t understand


van Kempen ZLE, Strijbis EMM, Al MMCT, Steenhuis M, Uitdehaag BMJ, Rispens T, Killestein J. SARS-CoV-2 Antibodies in Adult Patients With Multiple Sclerosis in the Amsterdam MS Cohort. JAMA Neurol. 2021 Apr 30. doi: 10.1001/jamaneurol.2021.1364.

This study looks at the Dutch experience of people getting infected with COVID-19 virus here are the results

A total of 1778 patients were contacted, and 546 patients were included (mean [SD] age, 46.9 [12.1] years; 388 women [71.1%]). In 64 patients (11.7%), SARS-CoV-2 antibodies were detected. Thirty-five patients experienced COVID-19, as established by polymerase chain reaction (PCR) testing. Of the patients positive by PCR, 4 (11%) tested negative for SARS-CoV-2 antibodies.

Nine patients who were antibody positive (14%) did not experience any symptoms suggestive of COVID-19……while only 14 of 482 patients (2.9%) without SARS-CoV-2 antibodies reported these symptoms. To our knowledge, there were no COVID-19 fatalities in this MS population. Of all 546 patients, 405 (74.2%) were receiving disease-modifying therapy. In these, SARS-CoV-2 antibodies were less prevalent in patients using injectable drugs (interferon β and glatiramer acetate) than patients with other treatments (3 of 69 [4%] vs 44 of 336 [13.1%]; P = .04). The median SARS-CoV-2 antibody response in patients treated with ocrelizumab was lower in comparison with other patients (0.2 [interquartile range, 0.1-0.4] nOD vs 2.5 [interquartile range, 0.6-2.5] nOD; P < .001;). All patients taking ocrelizumab were B-cell depleted, as measured at a median (range) of 2.5 (0-41) days before the antibody response was measured. None of these patients experienced hypogammaglobulinemia at that time.

Van Kempen et al

It is not surprising that people treated with ocrelizumab give a poor vaccination B cell response, because all indicators pointed in that direction, however this study does not give the expectation that fingolimod will give a poor vaccination response as was reported in early Israeli data. This study is consistent with cases reports from the natural infection. This is although there may be some blunting of the antibody response, many people make a response. The question has to be why this differenece?

Disclaimer: Please note that the opinions expressed here are those of the author and do not reflect the positions of the Barts and The London School of Medicine and Dentistry nor Barts Health NHS Trust or Queen Mary Univeristy of London.

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  • Did those taking flingolimod stop treatment while they were infected? If so, could they have recovered lymphocytes to make antibodies? I take Siponimod and my neuro had be stop treatment before and after each vaccine. I had antibody testing last week, but they ordered the wrong test! I’m hoping they’ll order the right one so that I know of the vaccine worked for me. Either way, this seems to be encouraging news for some.

  • I’m on Fingolimod and out of morbid curiosity I ignored Prof G’s advice (sorry!) and paid to have the antibody test just over two weeks after having my second Astra Zeneca vaccine. I came out as positive as had >50. 115 AU/ml to be exact. Was advised most folk are in the upper 1000s….as high as 80000. Comforting I am positive but as expected very low……

  • Not a doctor, but I was under the impression that fingolimod sequesters circulating lymphocytes but leaves tissue resident ones alone. Could that be a reason why a systemic infection might produce antibodies when a vaccine does not?

  • This study states that ‘SARS-COV-2 antibodies were less prevalent in patients using injectables drugs’.
    Why might this be? Also would you expect this to be true in people who have used injectables in the past and are no longer being treated?



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