The Coronavirus disease 2019 (COVID-19) pandemic due to severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection has brought significant challenges to our society during the last 2 years and continues to be a major health problem globally as new sub-variants emerge. Although effective vaccines were developed in record time and contributed to a significant decline in mortality and severe morbidity, the long-term consequences of SARS-CoV-2 infection are only now starting to be deciphered.
Evidence shows that COVID-19 could touch both peripheral as well as central nervous system (CNS) and is associated with a wide variety of neurological manifestations, ranging from psychiatric symptoms such as depression and anxiety, to meningitis, encephalitis, stroke, myopathies, or acute attacks of demyelinating diseases. Recent case reports and case series described the onset of CNS demyelinating disorders following COVID infection or vaccination, fulfilling the diagnostic criteria either for multiple sclerosis (MS), or MS-related disorders, such as acute disseminated encephalomyelitis (ADEM), neuromyelitis optica spectrum disorders (NMOSD), longitudinally-extensive transverse myelitis (LETM), myelin oligodendrocyte glycoprotein antibody disease (MOGAD), or were described as unclassified CNS inflammatory demyelinating diseases, in patients with no prior history of these diseases. While in vitro studies have demonstrated that SARS-Cov-2 has the ability to invade CNS and can infect neurons, glial cells, endothelial and choroid plexus cells, it is still not clear whether this hypothetical causal relation between the virus and demyelination is due to direct viral effects or are secondary to virus-induces immune dysregulation, ranging from increased proinflammatory cytokine production in the CNS to molecular mimicry or auto-antibody production.
This research topic aims to advance our knowledge on the possible link between COVID-19 and CNS demyelinating disorders. We welcome original research articles, reviews and mini-reviews, case series and prospective studies in relation to the following questions, but not limited to:
1) Could SARS-CoV-2 be considered a new (viral) risk factor for MS onset and/or relapses, and if so, could infection-related parameters such as severity of disease or number of reinfections be correlated with MS risk?
2) Conversely, could SARS-CoV-2 be considered a new (viral) risk factor for the onset of other demyelination disorders such as ADEM, NMOSD, LETM or MOGAD?
3) What is the prognosis of the COVID-19-related demyelinating diseases and how do they respond to current therapeutic strategies in comparison to non-COVID-19 cases?
4) What are the molecular mechanisms through which SARS-CoV-2 can initiate or potentiate an inflammatory attack and demyelination in the CNS, and how SARS-CoV-2 relate to other viruses associated with demyelinating diseases, such as EBV, in terms of pathogenic strategies.
5) What is the direct influence of SARS-CoV-2 on glial cells, namely astrocytes, microglia and oligodendrocytes?
6) Does SARS-CoV-2 have any potential to trigger and/or accelerate neurodegeneration and thus to contribute to MS progression?
The Coronavirus disease 2019 (COVID-19) pandemic due to severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection has brought significant challenges to our society during the last 2 years and continues to be a major health problem globally as new sub-variants emerge. Although effective vaccines were developed in record time and contributed to a significant decline in mortality and severe morbidity, the long-term consequences of SARS-CoV-2 infection are only now starting to be deciphered.
Evidence shows that COVID-19 could touch both peripheral as well as central nervous system (CNS) and is associated with a wide variety of neurological manifestations, ranging from psychiatric symptoms such as depression and anxiety, to meningitis, encephalitis, stroke, myopathies, or acute attacks of demyelinating diseases. Recent case reports and case series described the onset of CNS demyelinating disorders following COVID infection or vaccination, fulfilling the diagnostic criteria either for multiple sclerosis (MS), or MS-related disorders, such as acute disseminated encephalomyelitis (ADEM), neuromyelitis optica spectrum disorders (NMOSD), longitudinally-extensive transverse myelitis (LETM), myelin oligodendrocyte glycoprotein antibody disease (MOGAD), or were described as unclassified CNS inflammatory demyelinating diseases, in patients with no prior history of these diseases. While in vitro studies have demonstrated that SARS-Cov-2 has the ability to invade CNS and can infect neurons, glial cells, endothelial and choroid plexus cells, it is still not clear whether this hypothetical causal relation between the virus and demyelination is due to direct viral effects or are secondary to virus-induces immune dysregulation, ranging from increased proinflammatory cytokine production in the CNS to molecular mimicry or auto-antibody production.
This research topic aims to advance our knowledge on the possible link between COVID-19 and CNS demyelinating disorders. We welcome original research articles, reviews and mini-reviews, case series and prospective studies in relation to the following questions, but not limited to:
1) Could SARS-CoV-2 be considered a new (viral) risk factor for MS onset and/or relapses, and if so, could infection-related parameters such as severity of disease or number of reinfections be correlated with MS risk?
2) Conversely, could SARS-CoV-2 be considered a new (viral) risk factor for the onset of other demyelination disorders such as ADEM, NMOSD, LETM or MOGAD?
3) What is the prognosis of the COVID-19-related demyelinating diseases and how do they respond to current therapeutic strategies in comparison to non-COVID-19 cases?
4) What are the molecular mechanisms through which SARS-CoV-2 can initiate or potentiate an inflammatory attack and demyelination in the CNS, and how SARS-CoV-2 relate to other viruses associated with demyelinating diseases, such as EBV, in terms of pathogenic strategies.
5) What is the direct influence of SARS-CoV-2 on glial cells, namely astrocytes, microglia and oligodendrocytes?
6) Does SARS-CoV-2 have any potential to trigger and/or accelerate neurodegeneration and thus to contribute to MS progression?