B-cell depleting therapies may affect susceptibility to acute respiratory illness among patients with multiple sclerosis during the early COVID-19 epidemic in Iran

Abstract

To determine whether the course of COVID-19 is more severe in patients with MS and if MS diseasemodifying treatments (DMTs) affect the risk of contracting the disease. Methods: In a cross-sectional survey, data were collected by sending a questionnaire to 2000 patients with a demyelinating disease through an online portal system. Collected data included the current MS DMT and patientreported disability level, history of recent sick contact, recent fever, respiratory symptoms, diagnosis with COVID-19, and the disposition after the diagnosis. We defined a COVID-19-suspect group as patients having fever and cough or fever and shortness of breath, or a presumptive diagnosis based on suggestive chest computed tomography. We calculated the proportion of COVID-19-suspect patients and compared their demographics, clinical characteristics, and DMT categories with the rest of survey-responders, using univariable and multivariable models. Results: Out of 712 patients, 34 (4.8%) fulfilled our criteria for being in the COVID-19-suspect group. Only two patients required hospitalization. No patient required intensive care. In a multivariable model, disease duration (p-value=0.017), DMT category (p-value=0.030), and history of sick contact (p-values<0.001) were associated with the risk of being in the COVID-19-suspect group. Being on B-cell depleting antibodies (as compared to noncell depleting, non-cell trafficking inhibitor DMTs) was associated with a 2.6-fold increase in the risk of being in the COVID-19-suspect group. (RR: 3.55, 95%CI: 1.45, 8.68, p-value=0.005). Conclusions: The course of infection in patients with MS suspected of having COVID-19 was mild to moderate, and all patients had a full recovery. B-cell depleting antibodies may increase the susceptibility to contracting COVID-19.

Evaluation of the rate of COVID-19 infection, hospitalization and death among Iranian patients with multiple sclerosis

“…However, in another study in Iran, 712 patients with MS filled out a questionnaire about COVID-19 symptoms, of which 34 patients (4.8%) had COVID-19 symptoms. It was indicated that the use of B-cell depletion drugs can increase the risk of COVID-19 (Safavi et al, 2020), which is consistent with our findings. Increase in the risk of COVID-19 through B-cell depleting therapies was expected.…”

“…This study examines the rate of diagnosis of COVID-19 as well as the rate of hospitalization and prognosis in MS patients. In addition, our study assesses these ratios using a larger sample size and different patients from previous report from Iran (Safavi et al, 2020).…”

Major role of IgM in the neutralizing activity of convalescent plasma against SARS-CoV-2

“…Their use is associated with IgM deficiency in a substantial number of patients, while their impact on IgG and IgA levels is more limited (Kridin and Ahmed, 2020). In line with our data, recent studies reported that anti-CD20 therapy could be associated with a higher susceptibility to contract SARS-CoV-2 and develop severe COVID-19 (Guilpain et al, 2020;Hughes et al, 2020;Safavi et al, 2020;Schulze-Koops et al, 2020;Sharmeen et al, 2020;Sormani et al, 2020). Whether this is associated to the preferential depletion of IgM-producing B cells by these treatments (Looney et al, 2008) remains to be shown.…”

COVID-19 vaccine-readiness for anti-CD20-depleting therapy in autoimmune diseases

“…1), suggesting that most MS treatments that largely exhibit limited persistent effects on the innate immune and CD8 T cell responses would have limited influence on COVID‐19. SARS‐CoV‐2 is eliminated by the majority of people with MS and other autoimmunities on immunotherapies, without significant consequences [34–56] (Table 1). Anti‐viral antibodies, notably those targeting the receptor binding domain of the viral spike protein, clearly neutralize the virus [57,58] and can contribute to the elimination of the primary SARS‐CoV‐2 infection in humans [58,59].…”