Cladribine 2 Ocrelizumab 1/2

C

Prof G did a post cladribine 2, fingolimod 0 and there was one for ocrelizumab…this small study supports that result. Anti-CD20 clearly inhibits the antibody response towards the COVID-19 vaccine and and cladribine treated people responding well. All explained by Biology 101, I think. You give vaccine to people after the drug is long gone and what is there to response…responds. Treat whilst the drug is still present and depleting the B cells and you get a blunted B cell response.

Buttari F, Bruno A, Dolcetti E, Azzolini F, Bellantonio P, Centonze D, Fantozzi R. COVID-19 vaccines in multiple sclerosis treated with cladribine or ocrelizumab. Mult Scler Relat Disord. 2021 May 4;52:102983. doi: 10.1016/j.msard.2021.102983.

Since the recent approval of vaccines against COVID-19, efficacy concerns emerged for MS patients treated with immunosuppressive drugs. We report our experience in four patients, under cladribine (two) or under ocrelizumab (two) treatment, all with low lymphocyte count, three of them vaccinated after 3 months from the last dose with good immune response, one (under ocrelizumab) after 2 months, without developing an appropriate title of antibodies. This experience suggests that the discriminant for the response to the vaccine is not the lymphocyte count but the timing of the vaccination.

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

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MouseDoctor

13 comments

  • 2nd dose 10 weeks after Ocrevus might produce an effect then?

    Where do you get lymphocyte count, and where is it done?

    • Some people will respond ater 3-5 months but I fear this is going to be the minority, I predict about 20-25% and remmeber 5-10% have b cells back before 6 month dose. Lymphocyte counts will not be routine and so depends if these are done

        • Hope so be we need proof that ocre vaccinated individuals with covid-risk factors do OK….Most people on ocelizumab do OK away, so it would be the person doing badly that would appear.

          As for monoclonal pill we have this already inthe form of an injection in our covid study we have spotted someone from a trial

  • Mouse doctor do you feel optimist about having an antiviral targetting ebv approved for ms since there seems to be more ebv research ? For example the tenofovir alafenamide trial, the famciclovir trial, the moderna ebv vaccine and the t cell immunotherapy from atara biotherapeutics.

    • “optimist about having an antiviral targetting ebv”
      “since there seems to be more ebv research ?”

      https://www.google.com/search?q=anti+virals+for+ebv&rlz=1CATQWC_enUS898&oq=anti+virals+for+ebv&aqs=chrome..69i57j0i10j0i390l4.14259j0j15&sourceid=chrome&ie=UTF-8&safe=active&ssui=on

      No..probably never be an antiviral capable of removing EBV.
      Unfortunate as reason HSCT fails in long term is it targets ms disease process
      and not EBV directly.

      “Maybe the most important reason for the failure of antivirals for infectious mononucleosis therapy can be ascribed to the fact that the symptoms and signs of the disease are not the consequences of viral replication but the immunological response to EBV-infected B-cells that circulate in the blood and infiltrate the tissues of different organs. ”
      https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6429425/

      Probably t cell therapy…or..guided RNAs..is best bet..as drugs have limitations..this is why new
      EBV therapy/vaccine don’t come from old pharma..Merck/Pfizer.
      Moderna and Atara both started in 2010..and Atara doesn’t research EBV..they just took in hospital anti-EBV cancer t cell therapy and licensed it.

      “Anti-EBV therapy remains a major unmet medical need, in particular for patients with an impaired immune system…..A novel strategy that could potentially be used to combat both productive and latent EBV infections is the targeting of viral genetic elements required for viral fitness by CRISPR/Cas9 genome editing techniques. Lebbink’s group demonstrated that by simultaneous targeting of EBV genome with multiple guided RNAs (gRNAs), almost complete clearance of the virus from latently infected EBV-transformed cells was achieved. This opens new avenues for the development of therapeutic approaches to manage pathogenic human herpesviruses by means of novel genome-engineering technologies [117].”

  • Just came through to me on an email update of published papers.
    Pretty sure we have seen the data but thought people might like to see the peer reviewed version

    Humoral immune response to COVID-19 mRNA vaccine in patients with multiple sclerosis treated with high-efficacy disease-modifying therapies
    https://journals.sagepub.com/doi/full/10.1177/17562864211012835?utm_medium=email&utm_content=1A00574&utm_campaign=not+tracked&utm_term=&em=78262da6c53d13416b73b8dd3cf231b7b42429b11e615b907f991dabfe0544be&utm_source=adestra

  • Hi MD, off topic question but can we get a post on why MS is CNS only? Seeing that cells have to cross the BBB to attack the CNS, they are sure making a lot of effort instead of picking low hanging fruit (PNS).

    • Its not CNS only…Why because there is something in the CNS that is not in the PNS. MS-equivalent in the PNS is called something else. However one bigg difference you dont get oligodendrocytes in the PNS and I bet that has something to do with it

        • It is very clear that many people taking ocrelizumab do no seroconvert and and this is well less than 50% of people doing standard 6 month dosing. I have seen two studies from Israel showing seroconversion with cladribine the question is how close to injection can you get and still get a response.

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