What is known about the response to the COVID-19 vaccine in MS

Watching time: 6 minutes

For more coverage from CMSC 2022, click here. A transcript of the conversation below.

Matt Hoffman: I’m here with Dr. Daniel Kantor, sitting at CMSC.

Daniel Kantor, MD: Thank you for having me.

Matt Hoffman: I want to talk a little bit about your poster about the response to the COVID-19 vaccine for patients treated with ozanimod (Zeposia; Bristol Myers Squibb) and other S1P receptor modulators. To start from a point if you are not familiar with the work – Overview Overseas, how did we get to this point? What prompted this study?

Daniel Kantor, MD: What prompted the study was this virus called the coronavirus. The COVID-19 virus and the COVID-19 pandemic have raised many questions for the multiple sclerosis community. The first question was, is the MS community more vulnerable? The next question is, once there is a vaccine, what does that mean in terms of response to the vaccine?

For the first question, it seems generally, that people with multiple sclerosis are no more at risk than other people with other autoimmune diseases or, frankly, with other conditions in general. People who take certain medications may be at greater risk, and one of the things we’ve noticed is that when B cells are depleted or pushed — well, B cells are important in responding to viruses in response to vaccines. There are very common medications we use now for multiple sclerosis or ocrelizumab (Ocrevus, Genentech), we use ofatumumab (Kesimpta, Novartis), and some people still use rituximab (Rituxan; Genentech/Biogen). Those people seemed to have more severe COVID-19, possibly more intensive care unit visits, and so, the general question was, if given a vaccine, would they have the same responses as if it was someone without multiple sclerosis. any of those medicines.

The first part of this question is that many of us around the world were quick to try to answer it. Some people, what they did is they looked at their patients, and they looked at the case series, and they said, “Well, these people were taking these drugs, they got the vaccine, how many of them got COVID,” and others and so forth. There are clearly problems with this type of design. What we designed was a prospective study. The prospective study was looking at people who chose to get the vaccine anyway because not everyone chose to get the vaccine. But anyway, choose to get vaccinated, and then the question is, well, if we look at your pre-immune markers, your pre-lab scores, your pre-Questions, then after you get vaccinated and after you get the second vaccines, what happens when we go after those Persons for the rest of the year?

The way it was designed was actually to look specifically at one of the newer S1P receptor modulators. Many people remember the old, non-selective S1P receptor modulator, this drug Gilenya, or fingolimod. There have been other people’s questions and studies that have indicated that, well, not only do B cells seem to be a problem, it seems that if the immune cells are isolated within the lymphoid organs, it may not be good for the vaccine response. But maybe it’s different when you have no effect on S1P4. When you think of ozanimod, it’s selected for S1P1 and S1P5 – these two receptors, but not S1P4. Because of this, we’ll probably see some kind of different response. So, we wanted to test that.

The primary end point of the trial is the consideration of vaccine response. So, did they have a change in their response to spike protein immunoglobulin, and did it happen 4 weeks after the second vaccination. We have the data, it’s new, which is why it’s too late to break it. The data shows us that yes, in fact, when I gave it to people on ozanimod, 100% of the people actually came forward and got the response.

Then we look at the poster at other questions, and we also look at other disease-modifying factors. I wanted to do the study where we already have 30 patient subjects in each arm for each disease-modifying factor — but we’re lucky in MS. There are now more than 20 disease-modifying factors—depending on how they are calculated—depending on how they are calculated. So, we looked at 30 on ozanimod, and checked out 30 of all the other comers. When we looked at the other 30, what we saw is that if you ignore the first patient who was on fingolimod and then the three patients on ocrelizumab, then yes, those people also had a really good response. When I looked at people – and I don’t want to draw conclusions about 1 and 3 patients, it’s very hard to come up with any of them – but overall, the primary end point was really about ozanimod, and that actually showed an immune response.

Now, we didn’t just look at the immune response, we looked at the quantitative number of immune responses. What’s interesting is that the numbers are still protective. It is slightly lower than other drugs. So, a little less than in people taking glatiramer acetate (Copaxone, Teva), or interferon beta, for example, but they’re still protected. Then we also looked at T-cell markers. The problem now is, to do a really good study of T cells, you need fresh samples. This study was distributed all over the United States, and the idea was to have a virtual recording, and we’re sending blood transfusions to people’s homes. We can’t necessarily send it to a science lab that does amazing jobs in the T-cell response. But there is a company called Adaptive Biotechnologies that got an EUA — an emergency use authorization — to look at the T-cell response in a two-way: yes and no. It’s not made for a vaccine response, in fact to see if you have SARS-CoV-2 (COVID-19), but many of us also use it to look at a vaccine response. Remember, we don’t get a graded response, we just get a yes versus a no. Although patients treated with ozanimod had a lower, still protected, but lower antibody response, they still had protective T-cell responses. This was what was important in this study.

Text has been edited for clarity.


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