Acta Scientific Microbiology

Editorial Volume 7 Issue 10

Multiple Sclerosis in The Era of COVID-19 Pandemic and Long COVID-19 Condition

Attapon Cheepsattayakorn1-4*, Ruangrong Cheepsattayakorn5 and Porntep Siriwanarangsun2

1Faculty of Medicine Vajira Hospital, Navamindradhiraj University, Bangkok, Thailand
2Faculty of Medicine, Western University, Pathumtani Province, Thailand
310th Zonal Tuberculosis and Chest Disease Center, Chiang Mai, Thailand

4Department of Disease Control, Ministry of Public Health, Thailand
5Department of Pathology, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand

*Corresponding Author:Attapon Cheepsattayakorn, 10th Zonal Tuberculosis and Chest Disease Center, Chiang Mai, Thailand.

Received: July 24, 2024; Published: September 01, 2024

Citation: Attapon Cheepsattayakorn., et al. “Multiple Sclerosis in The Era of COVID-19 Pandemic and Long COVID-19 Condition". Acta Scientific Paediatrics 7.10 (2024):01-03.

Multiple sclerosis (MS), an autoimmune condition can damage the central nervous system (CNS) [1]. Persistence of various symptoms, such as anosmia, insomnia, brain fog, muscle pain, cough, dyspnea, exercise intolerance, fatigue, and chest pain after acute COVID-19 stage that has been denominated long COVID-19 condition or post-COVID-19 syndrome have been reported in many COVID-19 cases [2]. Additionally, antimicrobial usage that would change gastrointestinal microbiota composition is the principal risk factors, including COVID-19 severity for the development of long COVID-19 condition [3], whereas antimicrobials are the major gut-microbiota disruption [4]. Not well-controlled steroid therapy and poorly regulated glycemia are other risk factors for COVID-19-related mucormycosis [5]. In patients with moderate to severe COVID-19 disease, Guillain-Barre´ syndrome (GBS), encephalitis, meningitis, and acute necrotizing encephalopathy have been found [6], particularly increasing in hospital-admitted patients [7] and have been found in autopsy-deceased cases and expressing-human anti-converting-enzyme 2 (ACE 2), by neuro-invasion in cerebrospinal fluid (CSF) of a patient with GBS [8,9]. Hematogenous dissemination and direct-peripheral-neuron-endings invasion, particularly olfactory nerve that is located very close to the expressing-ACE2 and TMPRSS2-olfactory epithelium allowing easy COVID-19-initial replication are the two principal routes of neuro-invasion of COVID-19 [10,11]. The diagnosis of MS is usually depended on clinical manifestations (muscle weakness, muscle stiffness and spasms, coordination loss, vision impairment, pain, urinary bladder and bowel function changes due to damages of the myelin sheaths (Figure 1,2), CSF analysis for oligoclonal antibody band and inflammatory biomarkers, neuroimaging (multifocal and scattered lesions through the white and grey matter of the brain and spinal cord) [12].

Figure 1: Demonstrating immunopathogenesis of multiple sclerosis/experimental autoimmune encephalomyelitis. (A) Activation of self-reactive T cells specific for myelin antigens in secondary lymphoid organs, (B) licensing of self-reactive cells in the lungs and spleen (C), differentiation of Th17 cells in the intestine, (D) disruption of the blood–brain barrier and cell migration to the central nervous system, (E) local reactivation and expansion of Th cells, (F) local inflammatory process that leads to demyelination and neurodegeneration, (G) cells and molecules that mediate the control of disease via regulatory mechanisms [1]. CCL2 : C-C motif Chemokine Ligand 2; IL : Interleukin. Source: Created with Biorender.com.

Figure 1: Demonstrating immunopathogenesis of multiple sclerosis/experimental autoimmune encephalomyelitis. (A) Activation of self-reactive T cells specific for myelin antigens in secondary lymphoid organs, (B) licensing of self-reactive cells in the lungs and spleen (C), differentiation of Th17 cells in the intestine, (D) disruption of the blood–brain barrier and cell migration to the central nervous system, (E) local reactivation and expansion of Th cells, (F) local inflammatory process that leads to demyelination and neurodegeneration, (G) cells and molecules that mediate the control of disease via regulatory mechanisms [1]. CCL2 : C-C motif Chemokine Ligand 2; IL : Interleukin. Source: Created with Biorender.com.

Figure 2: Demonstrating the stages of MS immunopathogenesis which could be affected by SARS-CoV-2 [1]. BBB : Blood Brain Barrier. CNS : Central Nervous System. Source: Created with Biorender.com.

Figure 2: Demonstrating the stages of MS immunopathogenesis which could be affected by SARS-CoV-2 [1]. BBB : Blood Brain Barrier. CNS : Central Nervous System. Source: Created with Biorender.com.

In conclusion, a possible hyperactivation of both the Th1/Th17 axis and the NLRP3 inflammasome and type I interferon deficiency could cause MS aggravation. Role of vitamin D levels in the treatment of both diseases is not yet well-concluded.

Bibliography


Copyright: © 2024 Attapon Cheepsattayakorn., et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.