Inflammation and Epstein–Barr Virus at the Crossroads of Multiple Sclerosis and Post-Acute Sequelae of COVID-19 Infection
Recent studies have strengthened the evidence for Epstein–Barr Virus (EBV) as an important contributing factor in the development of multiple sclerosis (MS). Chronic inflammation is a key feature of MS. EBV<sup>+</sup> B cells can express cytokines and exosomes that promote inflammation,...
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| Format: | Article |
| Language: | English |
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MDPI AG
2023-04-01
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| Series: | Viruses |
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| Online Access: | https://www.mdpi.com/1999-4915/15/4/949 |
| _version_ | 1797603181610401792 |
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| author | Beth A. Rousseau Sumita Bhaduri-McIntosh |
| author_facet | Beth A. Rousseau Sumita Bhaduri-McIntosh |
| author_sort | Beth A. Rousseau |
| collection | DOAJ |
| description | Recent studies have strengthened the evidence for Epstein–Barr Virus (EBV) as an important contributing factor in the development of multiple sclerosis (MS). Chronic inflammation is a key feature of MS. EBV<sup>+</sup> B cells can express cytokines and exosomes that promote inflammation, and EBV is known to be reactivated through the upregulation of cellular inflammasomes. Inflammation is a possible cause of the breakdown of the blood–brain barrier (BBB), which allows the infiltration of lymphocytes into the central nervous system. Once resident, EBV<sup>+</sup> or EBV-specific B cells could both plausibly exacerbate MS plaques through continued inflammatory processes, EBV reactivation, T cell exhaustion, and/or molecular mimicry. Another virus, SARS-CoV-2, the cause of COVID-19, is known to elicit a strong inflammatory response in infected and immune cells. COVID-19 is also associated with EBV reactivation, particularly in severely ill patients. Following viral clearance, continued inflammation may be a contributor to post-acute sequelae of COVID-19 infection (PASC). Evidence of aberrant cytokine activation in patients with PASC supports this hypothesis. If unaddressed, long-term inflammation could put patients at risk for reactivation of EBV. Determining mechanisms by which viruses can cause inflammation and finding treatments for reducing that inflammation may help reduce the disease burden for patients suffering from PASC, MS, and EBV diseases. |
| first_indexed | 2024-03-11T04:25:47Z |
| format | Article |
| id | doaj.art-10a4fa7734964e67b73ce7ae4b891ef8 |
| institution | Directory Open Access Journal |
| issn | 1999-4915 |
| language | English |
| last_indexed | 2024-03-11T04:25:47Z |
| publishDate | 2023-04-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Viruses |
| spelling | doaj.art-10a4fa7734964e67b73ce7ae4b891ef82023-11-17T21:46:04ZengMDPI AGViruses1999-49152023-04-0115494910.3390/v15040949Inflammation and Epstein–Barr Virus at the Crossroads of Multiple Sclerosis and Post-Acute Sequelae of COVID-19 InfectionBeth A. Rousseau0Sumita Bhaduri-McIntosh1Division of Infectious Diseases, Department of Pediatrics, University of Florida, Gainesville, FL 32610, USADivision of Infectious Diseases, Department of Pediatrics, University of Florida, Gainesville, FL 32610, USARecent studies have strengthened the evidence for Epstein–Barr Virus (EBV) as an important contributing factor in the development of multiple sclerosis (MS). Chronic inflammation is a key feature of MS. EBV<sup>+</sup> B cells can express cytokines and exosomes that promote inflammation, and EBV is known to be reactivated through the upregulation of cellular inflammasomes. Inflammation is a possible cause of the breakdown of the blood–brain barrier (BBB), which allows the infiltration of lymphocytes into the central nervous system. Once resident, EBV<sup>+</sup> or EBV-specific B cells could both plausibly exacerbate MS plaques through continued inflammatory processes, EBV reactivation, T cell exhaustion, and/or molecular mimicry. Another virus, SARS-CoV-2, the cause of COVID-19, is known to elicit a strong inflammatory response in infected and immune cells. COVID-19 is also associated with EBV reactivation, particularly in severely ill patients. Following viral clearance, continued inflammation may be a contributor to post-acute sequelae of COVID-19 infection (PASC). Evidence of aberrant cytokine activation in patients with PASC supports this hypothesis. If unaddressed, long-term inflammation could put patients at risk for reactivation of EBV. Determining mechanisms by which viruses can cause inflammation and finding treatments for reducing that inflammation may help reduce the disease burden for patients suffering from PASC, MS, and EBV diseases.https://www.mdpi.com/1999-4915/15/4/949Epstein–Barr virusmultiple sclerosisCOVID-19post-acute sequelae of COVID-19 infectionPASCinflammation |
| spellingShingle | Beth A. Rousseau Sumita Bhaduri-McIntosh Inflammation and Epstein–Barr Virus at the Crossroads of Multiple Sclerosis and Post-Acute Sequelae of COVID-19 Infection Viruses Epstein–Barr virus multiple sclerosis COVID-19 post-acute sequelae of COVID-19 infection PASC inflammation |
| title | Inflammation and Epstein–Barr Virus at the Crossroads of Multiple Sclerosis and Post-Acute Sequelae of COVID-19 Infection |
| title_full | Inflammation and Epstein–Barr Virus at the Crossroads of Multiple Sclerosis and Post-Acute Sequelae of COVID-19 Infection |
| title_fullStr | Inflammation and Epstein–Barr Virus at the Crossroads of Multiple Sclerosis and Post-Acute Sequelae of COVID-19 Infection |
| title_full_unstemmed | Inflammation and Epstein–Barr Virus at the Crossroads of Multiple Sclerosis and Post-Acute Sequelae of COVID-19 Infection |
| title_short | Inflammation and Epstein–Barr Virus at the Crossroads of Multiple Sclerosis and Post-Acute Sequelae of COVID-19 Infection |
| title_sort | inflammation and epstein barr virus at the crossroads of multiple sclerosis and post acute sequelae of covid 19 infection |
| topic | Epstein–Barr virus multiple sclerosis COVID-19 post-acute sequelae of COVID-19 infection PASC inflammation |
| url | https://www.mdpi.com/1999-4915/15/4/949 |
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