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1.
Front Immunol ; 13: 931388, 2022.
Article in English | MEDLINE | ID: covidwho-2141951

ABSTRACT

Intracranial inoculation of the neuroadapted JHM strain of mouse hepatitis virus (JHMV) into susceptible strains of mice results in acute encephalomyelitis followed by a cimmune-mediated demyelination similar to the human demyelinating disease multiple sclerosis (MS). JHMV infection of transgenic mice in which expression of the neutrophil chemoattractant chemokine CXCL1 is under the control of a tetracycline-inducible promoter active within GFAP-positive cells results in sustained neutrophil infiltration in the central nervous system (CNS) that correlates with an increase in spinal cord demyelination. We used single cell RNA sequencing (scRNAseq) and flow cytometry to characterize molecular and cellular changes within the CNS associated with increased demyelination in transgenic mice compared to control animals. These approaches revealed the presence of activated neutrophils as determined by expression of mRNA transcripts associated with neutrophil effector functions, including CD63, MMP9, S100a8, S100a9, and ASPRV1, as well as altered neutrophil morphology and protein expression. Collectively, these findings reveal insight into changes in the profile of neutrophils associated with increased white matter damage in mice persistently infected with a neurotropic coronavirus.


Subject(s)
Demyelinating Diseases , Multiple Sclerosis , Murine hepatitis virus , White Matter , Animals , Central Nervous System , Chemokine CXCL1/metabolism , Humans , Matrix Metalloproteinase 9/metabolism , Mice , Mice, Transgenic , Multiple Sclerosis/metabolism , Neutrophils/metabolism , RNA, Messenger , Tetracyclines , White Matter/metabolism
2.
J Neuroinflammation ; 19(1): 267, 2022 Nov 04.
Article in English | MEDLINE | ID: covidwho-2108803

ABSTRACT

BACKGROUND: Triggering receptor expressed on myeloid cells 2 (Trem2) plays a protective role in neurodegenerative diseases. By contrast, Trem2 functions can exacerbate tissue damage during respiratory viral or liver infections. We, therefore, investigated the role of Trem2 in a viral encephalomyelitis model associated with prominent Th1 mediated antiviral immunity leading to demyelination. METHODS: Wild-type (WT) and Trem2 deficient (Trem2-/-) mice were infected with a sublethal glia tropic murine coronavirus (MHV-JHM) intracranially. Disease progression and survival were monitored daily. Leukocyte accumulation and pathological features including demyelination and axonal damage in spinal cords (SC) were determined by flow cytometry and tissue section immunofluorescence analysis. Expression of select inflammatory cytokines and chemokines was measured by RT-PCR and global myeloid cell gene expression in SC-derived microglia and infiltrated bone-marrow-derived macrophages (BMDM) were determined using the Nanostring nCounter platform. RESULTS: BMDM recruited to SCs in response to infection highly upregulated Trem2 mRNA compared to microglia coincident with viral control. Trem2 deficiency did not alter disease onset or severity, but impaired clinical recovery after onset of demyelination. Disease progression in Trem2-/- mice could not be attributed to altered virus control or an elevated proinflammatory response. A prominent difference was increased degenerated myelin not associated with the myeloid cell markers IBA1 and/or CD68. Gene expression profiles of SC-derived microglia and BMDM further revealed that Trem2 deficiency resulted in impaired upregulation of phagocytosis associated genes Lpl and Cd36 in microglia, but a more complex pattern in BMDM. CONCLUSIONS: Trem2 deficiency during viral-induced demyelination dysregulates expression of other select genes regulating phagocytic pathways and lipid metabolism, with distinct effects on microglia and BMDM. The ultimate failure to remove damaged myelin is reminiscent of toxin or autoimmune cell-induced demyelination models and supports that Trem2 function is regulated by sensing tissue damage including a dysregulated lipid environment in very distinct inflammatory environments.


Subject(s)
Brain , Demyelinating Diseases , Animals , Mice , Brain/metabolism , Phagocytosis/genetics , Microglia/metabolism , Demyelinating Diseases/chemically induced , Disease Progression , Gene Expression , Membrane Glycoproteins/genetics , Membrane Glycoproteins/metabolism , Receptors, Immunologic/genetics , Receptors, Immunologic/metabolism
3.
Mult Scler Relat Disord ; 67: 104175, 2022 Nov.
Article in English | MEDLINE | ID: covidwho-2105622

ABSTRACT

BACKGROUND: Clinical onset of multiple sclerosis (MSpostvacc) and myelin-oligodendrocyte-glycoprotein-antibody-associated disease (MOGADpostvacc) has been reported in association with SARS-CoV-2-vaccination. There is uncertainty as to whether this is causality (denovo disease) or temporal coincidence (manifestation of a preexisting, subclinical neuroinflammation). OBJECTIVES: Comparing the clinical characteristics of MSpostvacc-patients versus patients with MS (PwMS) whose clinical onset occurred independently of vaccination (MSreference). METHODS: Consecutive patients with clinical onset ≤30 days after SARS-CoV-2-vaccination were included. Clinical data, cerebrospinal fluid (CSF) parameters and magnetic resonance imaging (MRI) as well as optical coherence tomography (OCT) data were compared to an age- and sex-matched MSreference-cohort. RESULTS: We identified 5 MSpostvacc and 1 MOGADpostvacc patients who developed their clinical onset ≤ 30 days after SARS-CoV-2-vaccination. Clinical characteristics, CSF, MRI and OCT parameters from MSpostvacc patients were comparable to the MSreference cohort and showed evidence of preexisting subclinical CNS disease. The single case with MOGADpostvacc clearly differed from PwMS in higher CSF cell counts, remission of MRI lesions during follow-up, and absence of oligoclonal bands. CONCLUSIONS: Our case series indicates that MSpostvacc patients showed a rather typical initial manifestation in temporal association with SARS-CoV-2-vaccination and harbored preexisting subclinical neuroinflammation. This argues against the denovo development of MS in this cohort.


Subject(s)
COVID-19 Vaccines , COVID-19 , Demyelinating Diseases , Multiple Sclerosis , Humans , Autoantibodies , COVID-19/prevention & control , COVID-19 Vaccines/adverse effects , Demyelinating Diseases/chemically induced , Multiple Sclerosis/diagnostic imaging , Multiple Sclerosis/cerebrospinal fluid , SARS-CoV-2 , Vaccination/adverse effects
4.
Int J Mol Sci ; 23(19)2022 Sep 25.
Article in English | MEDLINE | ID: covidwho-2043776

ABSTRACT

Long-term neurological and mental complications of COVID-19, the so-called post-COVID syndrome or long COVID, affect the quality of life. The most persistent manifestations of long COVID include fatigue, anosmia/hyposmia, insomnia, depression/anxiety, and memory/attention deficits. The physiological basis of neurological and psychiatric disorders is still poorly understood. This review summarizes the current knowledge of neurological sequelae in post-COVID patients and discusses brain demyelination as a possible mechanism of these complications with a focus on neuroimaging findings. Numerous reviews, experimental and theoretical studies consider brain demyelination as one of the mechanisms of the central neural system impairment. Several factors might cause demyelination, such as inflammation, direct effect of the virus on oligodendrocytes, and cerebrovascular disorders, inducing myelin damage. There is a contradiction between the solid fundamental basis underlying demyelination as the mechanism of the neurological injuries and relatively little published clinical evidence related to demyelination in COVID-19 patients. The reason for this probably lies in the fact that most clinical studies used conventional MRI techniques, which can detect only large, clearly visible demyelinating lesions. A very limited number of studies use specific methods for myelin quantification detected changes in the white matter tracts 3 and 10 months after the acute phase of COVID-19. Future research applying quantitative MRI assessment of myelin in combination with neurological and psychological studies will help in understanding the mechanisms of post-COVID complications associated with demyelination.


Subject(s)
Attention Deficit Disorder with Hyperactivity , COVID-19 , Demyelinating Diseases , COVID-19/complications , Demyelinating Diseases/complications , Humans , Quality of Life
8.
Mult Scler Relat Disord ; 66: 104033, 2022 Oct.
Article in English | MEDLINE | ID: covidwho-1914839

ABSTRACT

BACKGROUND AND OBJECTIVE: The impact of COVID-19 infection and the effect of COVID-19 vaccinations on patients with demyelinating central nervous system disease in low middle income countries (LMIC's) have not been reported in detail earlier. We sought to identify risk factors associated with COVID-19 infection and the role of vaccination in order to develop management guidelines relevant to our patients. METHODS: A total of 621 patients from our registry that included 297 MS and 324 non MS disorders (Aquaporin- 4 antibody positive [50], Myelin oligodendrocyte glycoprotein antibody positive [81], seronegative [162] and clinically isolated syndrome [31]) were contacted. COVID-19 infection and vaccination status were queried. Patients who self reported COVID-19 infection based on a positive RT PCR report were compared with non infected patients to identify factors associated with susceptibility for COVID-19 infection. Univariate and multivariate analysis of potential risk factors included demographic and clinical features, body mass index (BMI), presence of comorbidities, absolute lymphocyte count, treatment types and vaccination status. RESULTS: Sixty seven patients with MS and 27 with non MS disorders developed COVID-19 infection. Among them 81 patients had mild infection and remained quarantined at home. All 13 patients who needed hospitalization recovered. Vaccination status was known in 582 patients among whom 69.8% had completed or taken one dose of vaccine at the time of inquiry. Majority of treated patients (61.3%) were on nonspecific immunosuppressants. In univariate analysis, presence of ≥1 comorbidity was significantly associated with COVID-19 infection in both MS (p value 0.01, OR-2.28, 95%CI- 1.18-4.4) and non MS patients (p- 0.001, OR-4.4, 95% CI-1.88-10.24). In the latter, BMI ≥ 30 (p-0.04, OR-3.27, 95% CI- 0.98-10.87) and EDSS score ≥ 3 (p-0.02, OR- 2.59,95% CI- 1.08-6.23) were other significant associations. History of prior COVID-19 vaccination was associated with reduced frequency of COVID-19 infection among MS (p- 0.001,OR- 0.24,95% CI- 0.13-0.43) and non MS patients (p- 0.0001,OR-0.14, 95% CI- 0.058-0.35). In multivariate analysis presence of comorbidities significantly increased and prior vaccination significantly reduced frequency of COVID-19 infection for both MS and related disorders. Concurrent disease modifying treatments showed a trend for association with infection. In the unvaccinated group, patients on disease modifying treatment were significantly at risk of infection, 81.5% unvaccinated and treated versus 18.5% who were unvaccinated and untreated (p- 0.0001, OR-10.1, 95% CI-0.56-2.11). CONCLUSION: Frequency and severity of COVID-19 infection was low among our patient cohort. Higher rate of infection in the treated group was significantly seen among unvaccinated patients. Our preliminary results suggests that in LMIC's, where "off label therapies" with inexpensive immunosuppressives are the main disease modifying drugs, mRNA vaccinations appear safe and effective against severe COVID-19 infection.


Subject(s)
Aquaporins , COVID-19 , Demyelinating Diseases , Multiple Sclerosis , Vaccines , Humans , COVID-19/epidemiology , COVID-19/prevention & control , COVID-19 Vaccines/administration & dosage , Demyelinating Diseases/drug therapy , Immunosuppressive Agents/therapeutic use , Multiple Sclerosis/drug therapy , Myelin-Oligodendrocyte Glycoprotein , Registries , RNA, Messenger , Vaccination/adverse effects , Vaccines/therapeutic use
10.
Viruses ; 14(4)2022 04 17.
Article in English | MEDLINE | ID: covidwho-1792411

ABSTRACT

Combined in silico, in vitro, and in vivo comparative studies between isogenic-recombinant Mouse-Hepatitis-Virus-RSA59 and its proline deletion mutant, revealed a remarkable contribution of centrally located two consecutive prolines (PP) from Spike protein fusion peptide (FP) in enhancing virus fusogenic and hepato-neuropathogenic potential. To deepen our understanding of the underlying factors, we extend our studies to a non-fusogenic parental virus strain RSMHV2 (P) with a single proline in the FP and its proline inserted mutant, RSMHV2 (PP). Comparative in vitro and in vivo studies between virus strains RSA59(PP), RSMHV2 (P), and RSMHV2 (PP) in the FP demonstrate that the insertion of one proline significantly resulted in enhancing the virus fusogenicity, spread, and consecutive neuropathogenesis. Computational studies suggest that the central PP in Spike FP induces a locally ordered, compact, and rigid structure of the Spike protein in RSMHV2 (PP) compared to RSMHV2 (P), but globally the Spike S2-domain is akin to the parental strain RSA59(PP), the latter being the most flexible showing two potential wells in the energy landscape as observed from the molecular dynamics studies. The critical location of two central prolines of the FP is essential for fusogenicity and pathogenesis making it a potential site for designing antiviral.


Subject(s)
Demyelinating Diseases , Spike Glycoprotein, Coronavirus , Animals , Mice , Peptides/metabolism , Proline , Spike Glycoprotein, Coronavirus/genetics , Spike Glycoprotein, Coronavirus/metabolism , Viral Envelope Proteins/metabolism
11.
Mult Scler Relat Disord ; 60: 103739, 2022 Apr.
Article in English | MEDLINE | ID: covidwho-1747671

ABSTRACT

BACKGROUND: ChAdOx1-S (Covishield™/Vaxzervria, AstraZeneca) and BBV152 (Covaxin) SARS-CoV-2 vaccines are proven to be safe and effective, but rare complications have been reported. OBJECTIVE: To describe reports of central nervous system (CNS) demyelination following ChAdOx1-S and BBV152 vaccinations. METHODS & RESULTS: We report 29 (17 female; mean 38 years) cases of CNS demyelination; twenty-seven occurred in temporal association with ChAdOx1-S vaccine; two in association with BBV152 vaccine. Eleven patients had presentation with myelitis, six patients developed optic neuritis, five had acute demyelinating encephalomyelitis, three presented with brainstem demyelination, and four had multiaxial involvement. Myelin oligodendrocyte glycoprotein (MOG) antibodies were positive in ten patients. One patient with ADEM and tumefactive demyelinating lesions died after a prolonged intensive care unit stay and superimposed infection. As compared to the control group (87); the postvaccinial cases were found to have a significantly higher mean age, presence of encephalopathy (p value:0.0007), CSF pleocytosis (p value: 0.0094) and raised CSF protein (p value: 0.0062). CONCLUSIONS: It is difficult to establish a causal relationship between vaccination and neurological adverse events such as demyelination. The temporal association with the vaccination and the presence of MOG antibodies raises the possibility of an immunogenic process triggered by the vaccine in susceptible individuals.


Subject(s)
COVID-19 , Demyelinating Diseases , Autoantibodies , COVID-19/prevention & control , COVID-19 Vaccines/adverse effects , Demyelinating Diseases/chemically induced , Female , Humans , Myelin-Oligodendrocyte Glycoprotein , SARS-CoV-2
12.
Curr Top Med Chem ; 22(16): 1369-1378, 2022.
Article in English | MEDLINE | ID: covidwho-1731667

ABSTRACT

The SARS-CoV-2 virus is responsible for COVID-19 affecting millions of humans around the world. COVID-19 shows various clinical symptoms (fever, cough, fatigue, diarrhea, body aches, headaches, anosmia, and hyposmia). Approximately 30% of patients with COVID-19 showed neurological symptoms, from mild to severe manifestations including headache, dizziness, impaired consciousness, encephalopathy, anosmia, hypogeusia, and hyposmia, among others. The neurotropism of the SARS-CoV-2 virus explains its neuroinvasion provoking neurological damage such as acute demyelination, neuroinflammation, etc. At the molecular level, the COVID-19 patients had higher levels of cytokines and chemokines known as cytokines storms which disrupt the blood-brain barrier allowing the entrance of monocytes and lymphocytes, causing neuroinflammation, neurodegeneration, and demyelination. In addition, the proinflammatory cytokines have been observed in ischemic, hemorrhagic strokes, seizures, and encephalopathy. In this sense, early neuroprotective management should be adopted to avoid or decrease neurological damage due to SARS-CoV-2 infection. Several approaches can be used; one of them includes using HDAC inhibitors (HDACi) due to their neuroprotective effects. Also, the HDACi down-regulates the proinflammatory cytokines (IL-6 and TNF-α) decreasing the neurotoxicity. HDACi can also avoid and prevent the entrance of the virus into the central nervous System (CNS) and decrease the virus replication by downregulating the virus receptors. Here we review the mechanisms that could explain how the SARS-CoV-2 virus could reach the CNS, induce neurological damage and symptoms, and the possibility to use HDACi as neuroprotective therapy.


Subject(s)
Brain Diseases , COVID-19 , Demyelinating Diseases , Nervous System Diseases , Anosmia , COVID-19/drug therapy , Cytokines , Demyelinating Diseases/complications , Humans , Neuroprotection , SARS-CoV-2
13.
Neurol India ; 70(1): 409-411, 2022.
Article in English | MEDLINE | ID: covidwho-1726256

ABSTRACT

Background: Postmarketing surveillance of COVID-19 vaccination reveals that the COVID-19 vaccine administration is associated with several rare but serious neurological complications. Case Report: We report a case of new-onset tumefactive demyelinating brain lesion that developed after administration of an adenovector-based COVID-19 vaccine. A middle-aged female presented with recent right hemiparesis, which was noticed 2 days after she received the first dose of the vaccine. Magnetic resonance imaging (MRI) revealed a large subcortical T2/FLAIR hyperintensities involving corpus callosum as well. The patient responded to oral methylprednisolone. At 4 weeks, a follow-up MRI revealed a reduction in size of the lesion. Conclusion: To conclude, adenovector-based COVID-19 vaccination may be associated with a tumefactive demyelinating lesion.


Subject(s)
COVID-19 Vaccines , COVID-19 , Demyelinating Diseases/chemically induced , Adenoviridae , Brain/diagnostic imaging , Brain/pathology , COVID-19/prevention & control , COVID-19 Vaccines/adverse effects , Corpus Callosum/diagnostic imaging , Corpus Callosum/pathology , Female , Humans , Magnetic Resonance Imaging , Methylprednisolone/therapeutic use , Middle Aged , SARS-CoV-2
14.
Brain Behav Immun ; 87: 34-39, 2020 07.
Article in English | MEDLINE | ID: covidwho-1719335

ABSTRACT

The coronavirus disease 19 (COVID-19) pandemic is a significant psychological stressor in addition to its tremendous impact on every facet of individuals' lives and organizations in virtually all social and economic sectors worldwide. Fear of illness and uncertainty about the future precipitate anxiety- and stress-related disorders, and several groups have rightfully called for the creation and dissemination of robust mental health screening and treatment programs for the general public and front-line healthcare workers. However, in addition to pandemic-associated psychological distress, the direct effects of the virus itself (several acute respiratory syndrome coronavirus; SARS-CoV-2), and the subsequent host immunologic response, on the human central nervous system (CNS) and related outcomes are unknown. We discuss currently available evidence of COVID-19 related neuropsychiatric sequelae while drawing parallels to past viral pandemic-related outcomes. Past pandemics have demonstrated that diverse types of neuropsychiatric symptoms, such as encephalopathy, mood changes, psychosis, neuromuscular dysfunction, or demyelinating processes, may accompany acute viral infection, or may follow infection by weeks, months, or longer in recovered patients. The potential mechanisms are also discussed, including viral and immunological underpinnings. Therefore, prospective neuropsychiatric monitoring of individuals exposed to SARS-CoV-2 at various points in the life course, as well as their neuroimmune status, are needed to fully understand the long-term impact of COVID-19, and to establish a framework for integrating psychoneuroimmunology into epidemiologic studies of pandemics.


Subject(s)
Coronavirus Infections/psychology , Cytokine Release Syndrome/psychology , Mental Disorders/psychology , Nervous System Diseases/psychology , Pneumonia, Viral/psychology , Acute Disease , Anxiety/etiology , Anxiety/immunology , Anxiety/psychology , Bacterial Translocation , Betacoronavirus , COVID-19 , Chronic Disease , Coronavirus Infections/complications , Coronavirus Infections/immunology , Coronavirus Infections/therapy , Cytokine Release Syndrome/immunology , Cytokine Release Syndrome/therapy , Demyelinating Diseases/etiology , Demyelinating Diseases/immunology , Demyelinating Diseases/physiopathology , Demyelinating Diseases/psychology , Depression/etiology , Depression/immunology , Depression/psychology , Humans , Immunologic Factors/adverse effects , Mental Disorders/etiology , Mental Disorders/immunology , Mental Health , Nervous System Diseases/etiology , Nervous System Diseases/immunology , Nervous System Diseases/physiopathology , Neurodegenerative Diseases/etiology , Neurodegenerative Diseases/immunology , Neurodegenerative Diseases/physiopathology , Neurodegenerative Diseases/psychology , Pandemics , Pneumonia, Viral/complications , Pneumonia, Viral/immunology , Pneumonia, Viral/therapy , Psychoneuroimmunology , Psychotic Disorders/etiology , Psychotic Disorders/immunology , Psychotic Disorders/psychology , Public Health , SARS-CoV-2 , Stress Disorders, Post-Traumatic/etiology , Stress Disorders, Post-Traumatic/immunology , Stress Disorders, Post-Traumatic/psychology
15.
Hum Vaccin Immunother ; 17(11): 4099-4101, 2021 Nov 02.
Article in English | MEDLINE | ID: covidwho-1621488

ABSTRACT

Vaccination-induced demyelination is a rare, unusual side effect of certain vaccines which can cause significant damage to patient's sensory-motor abilities within days. Although COVID-19 vaccines go through rigorous clinical trials before they are injected to the general population, certain unexpected side effects remain inevitable. We herein describe a case of a 42-year-old woman who experienced acute demyelination 10 days after the Oxford-AstraZeneca vaccination. To the best of our knowledge, this is the first case of such nature and severity described regarding COVID-19 vaccines' side effects.


Subject(s)
COVID-19 , Cerebellar Ataxia , Demyelinating Diseases , Adult , COVID-19 Vaccines , Demyelinating Diseases/chemically induced , Demyelinating Diseases/diagnosis , Female , Humans , SARS-CoV-2 , Vaccination/adverse effects
16.
Neurol India ; 69(5): 1424-1426, 2021.
Article in English | MEDLINE | ID: covidwho-1502579

ABSTRACT

BACKGROUND: The ongoing Coronavirus disease-19 (COVID-19) pandemic has revealed a plethora of extrapulmonary manifestations including neurological presentations. To date, nervous system demyelination has been relatively infrequently reported in this setting. Also, while most data point toward immune activation as a causative process, few studies propound a direct effect. CASE DESCRIPTION: A 35-year-old man presented with severe new-onset headache, hemiparesis, and focal seizures culminating in deeply altered sensorium. Radiological evaluation showed a large expansile demyelinating lesion in the right cerebral hemisphere. Nasopharyngeal swab COVID reverse transcription-polymerase chain reaction (RT-PCR) was positive. After initial non-response to steroids, the patient responded well to plasma exchange leading to complete recovery. CONCLUSIONS: This report highlights a case of active severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection presenting with tumefactive demyelination and subsequent response to therapy. It is important to recognize atypical presentations at this juncture as it may be crucial for planning treatment strategies.


Subject(s)
COVID-19 , Demyelinating Diseases , Adult , Demyelinating Diseases/diagnostic imaging , Humans , Male , Pandemics , SARS-CoV-2
19.
J Neurovirol ; 27(4): 656-661, 2021 08.
Article in English | MEDLINE | ID: covidwho-1260618

ABSTRACT

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) commonly results in a respiratory illness in symptomatic patients; however, those critically ill can develop a leukoencephalopathy. We describe two patients who had novel subacute MRI findings in the context of coronavirus disease 2019 (COVID-19) leukoencephalopathy, which we hypothesize could implicate a potent small-vessel vasculitis, ischemic demyelination and the presence of prolonged ischemia. Recent evidence of the direct neuroinvasiness of SARS-CoV-2 leading to ischemia and vascular damage supports this hypothesis.


Subject(s)
COVID-19/complications , Demyelinating Diseases/pathology , Leukoencephalopathies/pathology , Leukoencephalopathies/virology , Vasculitis, Central Nervous System/pathology , Demyelinating Diseases/virology , Female , Humans , Magnetic Resonance Imaging , Male , Middle Aged , SARS-CoV-2 , Vasculitis, Central Nervous System/virology
20.
Acta Neurol Belg ; 121(4): 859-866, 2021 Aug.
Article in English | MEDLINE | ID: covidwho-1208875

ABSTRACT

The coronavirus disease of 2019 (COVID-19) is caused by the severe acute respiratory syndrome coronavirus-2 (SARS CoV-2), that already appeared as a global pandemic. Presentation of the disease often includes upper respiratory symptoms like dry cough, dyspnea, chest pain, and rhinorrhea that can develop to respiratory failure, needing intubation. Furthermore, the occurrence of acute and subacute neurological manifestations such as stroke, encephalitis, headache, and seizures are frequently stated in patients with COVID-19. One of the reported neurological complications of severe COVID-19 is the demolition of the myelin sheath. Indeed, the complex immunological dysfunction provides a substrate for the development of demyelination. Nevertheless, few published reports in the literature describe demyelination in subjects with COVID-19. In this short narrative review, we discuss probable pathological mechanisms that may trigger demyelination in patients with SARS-CoV-2 infection and summarize the clinical evidence, confirming SARS-CoV-2 condition as a risk factor for the destruction of myelin.


Subject(s)
COVID-19/complications , COVID-19/immunology , Demyelinating Diseases/virology , Humans , SARS-CoV-2
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