Approach to SARS-CoV-2 Vaccination in Patients With Multiple Sclerosis

Abstract

For more than a year now, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has been causing the coronavirus disease (COVID-19) pandemic with high mortality and detrimental effects on society, economy, and individual lives. Great hopes are being placed on vaccination as one of the most potent escape strategies from the pandemic and multiple vaccines are already in clinical use. However, there is still a lot of insecurity about the safety and efficacy of vaccines in patients with autoimmune diseases like multiple sclerosis (MS), especially under treatment with immunomodulatory or immunosuppressive drugs. We propose strategic approaches to SARS-CoV-2 vaccination management in MS patients and encourage fellow physicians to measure the immune response in their patients. Notably, both humoral and cellular responses should be considered since the immunological equivalent for protection from SARS-CoV-2 after infection or vaccination still remains undefined and will most likely involve antiviral cellular immunity. It is important to gain insights into the vaccine response of immunocompromised patients in order to be able to deduce sensible strategies for vaccination in the future.

Keywords: CD20; coronavirus disease (COVID-19); immune response; immunomodulation; immunotherapy; multiple sclerosis; severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2); vaccination.

Figure 1

Open questions concerning SARS-CoV-2 vaccination in MS patients. Several issues regarding the vaccination against COVID-19 in MS patients still need to be addressed by further studies. For one, it is not clear, whether vaccination is as efficacious in patients receiving immunomodulating therapies as it is in healthy people. Second, the immunological equivalent of a protective immune response to vaccination has not been determined yet – are B cells and antibodies essential, is a specific T cell response needed? Furthermore, the durability of immune responses after vaccination is unknown. Lastly, it needs to be observed whether SARS-CoV-2 generates mutants that escape protection of a vaccine-elicited immune response.

Figure 2

Current understanding of the adaptive immune response to SARS-CoV-2 infection. Upon infection with SARS-CoV-2, the virus replicates in the human host and hence antigen load increases. Virus-specific T cells are generated and fight the virus so that antigen load decreases. Simultaneously, B cells differentiate into plasma cells which produce antiviral antibodies. A part of the secreted antibodies have neutralizing capacities. Memory B cells emerge which can secrete specific antibodies more rapidly upon rechallenge with the antigen. All of the aforementioned agents of the immune system decrease over time. However, the long-term kinetics of this decrease and the response to a possible repeated viral challenge at various time points are not known. Figure adapted with permission from (92, 93).