Immunology of COVID-19 and disease-modifying therapies: The good, the bad and the unknown.
Eur J Neurol
; 28(10): 3503-3516, 2021 Oct.
Article
in English
| MEDLINE | ID: covidwho-1608969
ABSTRACT
OBJECTIVE:
The outbreak of the SARS-CoV-2 pandemic, caused by a previously unknown infectious agent, posed unprecedented challenges to healthcare systems and unmasked their vulnerability and limitations worldwide. Patients with long-term immunomodulatory/suppressive therapies, as well as their physicians, were and are concerned about balancing the risk of infection and effects of disease-modifying therapy. Over the last few months, knowledge regarding SARS-CoV-2 has been growing tremendously, and the first experiences of infections in patients with multiple sclerosis (MS) have been reported.METHODS:
This review summarizes the currently still limited knowledge about SARS-CoV-2 immunology and the commonly agreed modes of action of approved drugs in immune-mediated diseases of the central nervous system (MS and neuromyelitis optica spectrum disorder). Specifically, we discuss whether immunosuppressive/immunomodulatory drugs may increase the risk of SARS-CoV-2 infection and, conversely, may decrease the severity of a COVID-19 disease course.RESULTS:
At present, it can be recommended in general that none of those therapies with a definite indication needs to be stopped per se. A possibly increased risk of infection for most medications is accompanied by the possibility to reduce the severity of COVID-19.CONCLUSIONS:
Despite the knowledge gain over the last few months, current evidence remains limited, and, thus, further clinical vigilance and systematic documentation is essential.Keywords
Full text:
Available
Collection:
International databases
Database:
MEDLINE
Main subject:
Neuromyelitis Optica
/
COVID-19
/
Multiple Sclerosis
Type of study:
Observational study
/
Prognostic study
/
Qualitative research
/
Systematic review/Meta Analysis
Limits:
Humans
Language:
English
Journal:
Eur J Neurol
Journal subject:
Neurology
Year:
2021
Document Type:
Article
Affiliation country:
Ene.14578
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