Pathogenesis of Neurological Disorders Associated with Coronavirus Infections and Post-acute Sequelae of COVID-19

A special issue of Pathogens (ISSN 2076-0817). This special issue belongs to the section "Viral Pathogens".

Deadline for manuscript submissions: closed (31 January 2025) | Viewed by 1022

Special Issue Editor


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Guest Editor
Department of Microbiology and Immunology, College of Medicine, University of Arkansas for Medical Sciences, Little Rock, AR, USA
Interests: coronaviruses; pathogenesis; virus–host interaction; antivirals; rapid virus detection

Special Issue Information

Dear Colleagues,

The World Health Organization (WHO) declared the coronavirus disease (COVID-19) caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) a pandemic in 2020. Although COVID-19 primarily targets the respiratory system, it can also affect other organs, including the nervous system. Common reported neurological symptoms in COVID-19 patients include headache, seizures, ataxia, acute cerebrovascular disease, stroke, impaired consciousness, hyposmia and hypogeusia or even loss of smell and taste, neuralgias and Guillain–Barré syndrome.

Acute COVID-19 can sometimes lead to long-lasting effects, known as long COVID or post-COVID conditions (PCC). Some people have symptoms of COVID-19 that last for months or even years after their initial infection. Some may develop new symptoms after an initial recovery or after mild initial COVID-19. Long COVID can include a wide variety of symptoms in the nervous system that range from a loss of smell and taste, impaired concentration, fatigue, pain, sleep disorders, autonomic disorders and headache to psychological effects such as depression or psychosis. It is estimated that about 10–20% of patients infected by SARS-CoV-2 may develop long COVID. Although the exact numbers of those living with long COVID are uncertain, given the large numbers of COVID-19 cases worldwide, the long-term impact on individuals, public health, societies and global economy is enormous.

Therefore, understanding the full extent of COVID-19-associated neurological complications and their causes, as well as their underlying mechanisms of pathogenesis is crucial for the development of diagnostic tools and effective therapeutic interventions.

In this Special Issue, we seek manuscripts focusing on the causes and pathogenesis of neurological disorders associated with both acute and post-acute COVID-19. We also seek manuscripts describing research findings on neurological disorders caused by SARS-CoV-2 and other coronavirus infections using experimental and animal model systems. Both research and review articles are welcome.

Prof. Dr. Xuming Zhang
Guest Editor

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Keywords

  • coronaviruses
  • pathogenesis
  • neurological disorders
  • COVID-19
  • long COVID

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Published Papers (1 paper)

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Research

22 pages, 6156 KiB  
Article
Extensive T-Cell Profiling Following SARS-CoV-2 mRNA Vaccination in Multiple Sclerosis Patients Treated with DMTs
by Hannah Solchenberger, Marcus Odendahl, Dirk Schriefer, Undine Proschmann, Georges Katoul al Rahbani, Tjalf Ziemssen and Katja Akgün
Pathogens 2025, 14(3), 235; https://doi.org/10.3390/pathogens14030235 - 27 Feb 2025
Viewed by 606
Abstract
Disease-modifying therapies (DMTs) are known to impact cellular and humoral immune response in persons with multiple sclerosis (pwMS). In this study, we performed in-depth SARS-CoV-2-specific T-cell profiling using flow cytometry. T-cell immunity in pwMS with or without DMTs was evaluated before a first [...] Read more.
Disease-modifying therapies (DMTs) are known to impact cellular and humoral immune response in persons with multiple sclerosis (pwMS). In this study, we performed in-depth SARS-CoV-2-specific T-cell profiling using flow cytometry. T-cell immunity in pwMS with or without DMTs was evaluated before a first SARS-CoV-2 messenger ribonucleic acid (mRNA) vaccination and at one-, two- and six-month follow-up. T-cell stimulation without SARS-CoV-2-specific antigens was used as a control. T-cell response was compared to B-cell response by evaluating SARS-CoV-2-specific antibodies. We observed an upregulation of specific subpopulations of SARS-CoV-2 spike-specific CD4+ T cells. Thus, our results demonstrate the induction of a broad and distinct CD4+ T-cell response in pwMS even on anti-CD20 treatment and sphingosine-1-phosphate receptor modulation after SARS-CoV-2 mRNA vaccination. This was particularly seen in CD4+high and CD4+CD154+ T cells. Our results do not support the induction of a CD8+ T-cell immune response. While humoral immune response was impaired in pwMS during ocrelizumab and fingolimod treatment, there was evidence of a compensatory upregulation of subpopulations of SARS-CoV-2-specific CD4+ T cells at low levels of seroconversion in pwMS. In conclusion, our results provide important insights into the mechanisms of the adaptive immune response in pwMS following SARS-CoV-2 mRNA vaccination. Full article
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