Abstract

The purpose of this review is to examine whether there is a possible (etiological/triggering) relationship between infection with various Coronaviruses, including Severe Acute Respiratory Syndrome-related Coronavirus-2 (SARS-CoV-2), the virus responsible for the Coronavirus disease-19 (Covid-19) pandemia, and Multiple Sclerosis (MS), and whether an increase of the prevalence of MS after the current Covid-19 pandemia should be expected, examining new and preexisting data. Although the exact pathogenesis of MS remains unknown, environmental agents seem to greatly influence the onset of the disease, with viruses being the most popular candidate. Existing data support this possible etiological relationship between viruses and MS, and experimental studies show that Coronaviruses can actually induce an MS-like demyelinating disease in animal models. Findings in MS patients could also be compatible with this coronaviral MS hypothesis. More importantly, current data from the Covid-19 pandemia show that SARS-CoV-2 can trigger autoimmunity and possibly induce autoimmune diseases, in the Central Nervous System as well, strengthening the viral hypothesis of MS. If we accept that Coronaviruses can induce MS, it is reasonable to expect an increase in the prevalence of MS after the Covid-19 pandemia. This knowledge is of great importance in order to protect the aging groups that are more vulnerable against autoimmune diseases and MS specifically, and to establish proper vaccination and health policies.

Highlights

  • The first coronavirus (CoV), Infectious Bronchitis Virus (IBV), was isolated in the 1930s, as the etiologic agent of a highly transmittable respiratory disease in chicken (Lalchhandama 2020; Schochetman et al 1977; Tyrrell et al 1975), and since a plethora of diseases in many species of birds and mammals have been reported (Durham et al 1979)

  • The purpose of this review is to examine whether there is a possible relationship between infection with various Coronaviruses, including Severe Acute Respiratory Syndrome-related Coronavirus-2 (SARS-CoV-2), the virus responsible for the Coronavirus disease-19 (Covid-19) pandemia, and Multiple Sclerosis (MS), and whether an increase of the prevalence of MS after the current Covid-19 pandemia should be expected, examining new and preexisting data

  • The occurrence of the Covid-19 pandemia, the impact that CoVs and SARS-CoV-2 seem to have on the activation of autoimmunity, and the ability of CoVs to lead to demyelination in the central nervous system (CNS), have brought the viral hypothesis of MS to the consideration again

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Summary

Introduction

The first coronavirus (CoV), Infectious Bronchitis Virus (IBV), was isolated in the 1930s, as the etiologic agent of a highly transmittable respiratory disease in chicken (Lalchhandama 2020; Schochetman et al 1977; Tyrrell et al 1975), and since a plethora of diseases in many species of birds and mammals have been reported (Durham et al 1979). The virus causing the disease was named JHM, after Dr John Howard Mueller (Pappenheimer 1958) It was later identified as the neurotropic strain of the Murine Hepatitis Virus (MHV), discovered years later (Herndon et al 1975; Lalchhandama 2020), and it is the main CoV used in the animal projects in order to induce and study demyelination in the CNS. Some of the first detections of CoVs in human tissues came from samples of MS patients, and this expectedly further raised the question of whether this finding was just coincidental or not, the suspicion that CoVs may be associated to MS had already been expressed, due to their ability to induce demyelination in experimental animal models As it is evident, CoVs have been associated with MS even from the first years of their appearance in the foreground. The following “forgotten” question resurfaces again: is there a causal relationship between CoVs and demyelinating diseases, and MS in particular? In this review, we aim to answer this question, by describing and summarizing all the existing and recent data

MS pathogenesis
Possible mechanisms
Cerebrospinal fluid
Brain tissue
Common elements with MS
Findings
Conclusions
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