There is a proven association between HCoV and MS pathogenesis which has evolved from several experimental studies which revealed that murine coronavirus infection of susceptible mice led to an inflammatory demyelination similar to MS; coronavirus RNA sequences and its antigen were detected in demyelinating lesions [4]; two HCoV strains were studied in the brains of patients with MS (pwMS); HCoV-229E viral RNA was detectable in the CNS of 36% pwMS and in none of those with other neurological diseases and normal controls, whereas no HCoV-OC43 nucleic acid was detected in any of the specimens; and HCoV-myelin cross-reactive T cell lines were predominantly found in pwMS compared to patients with other neurological diseases or healthy controls. Moreover, the cross-reactivity observed appears to be found in MS but not in other inflammatory or neurological disorders. Molecular mimicry could be the mechanism through activation of myelin-reactive T cells by a virus infection in a genetically predisposed individual [1].
Furthermore, coronavirus neurotropism has been demonstrated in humans; an acute infection by HCoV was detected in cultures of human microglia, astrocytes, and oligodendrocytes; also, a persistent infection was demonstrated in cell lines from nervous system [1]. Neurological manifestations have been reported as a result of SARS-CoV-2 systemic infection, and the access can be either hematological or neuronal via olfactory nerve [5]; however, neurotropism is not established yet for the SARS-CoV-2.
Based on the aforementioned data, during the current COVID-19 pandemic and the emergence of the corona virus strains, two concerns are worth considering; the possibility of increasing MS, as well as other neurological autoimmune disorders, incidence worldwide in the coming years; however, no solid conclusions can be drawn regarding this possibility, as different strains can exhibit various characteristics as evidenced by the probable association of HCoV-229E to MS pathology and the absence of such association in the HCoV-OC43 strain [1], and still the behavior of SARS-CoV-2 is being explored; the other concern is reconsideration of the use of natalizumab, which is considered relatively safe being not a cause of peripheral lymphopenia, but inducing its effect centrally by preventing activated auto-reactive T cell trafficking into the CNS [6], meanwhile, we may be faced by a neurotropic virus whose effects may be revealed in the coming future.