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The Role of SARS-CoV-2 in Immunomodulation—Post-Pandemic Reflection on the Role of Viruses in Human Immunology

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: 20 September 2025 | Viewed by 3689

Special Issue Editor

Dr. Katarzyna A. Lisowska

E-Mail Website
Guest Editor
Department of Physiopathology, Faculty of Medicine, Medical University of Gdańsk, 80-210 Gdańsk, Poland
Interests: T cells; B cells; inflammation; immunomodulation; autoimmune diseases; kidney diseases; depression
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The SARS-CoV-2 pandemic was a surprise for the whole world but also an excellent opportunity to take a closer look at the role of viruses in human immunology. The diverse picture of clinical symptoms and the impact of comorbidities on the course of COVID-19 has proven how little we still know about the impact of viruses on the behavior of the immune system. Immune cells are responsible for protecting our body against viral infections. However, many viruses can modulate the immune responses, unfavorably affecting the infected person’s immunology. Viruses can affect the host in various ways, ranging from minimal impact to severely damaging states. A perfect example is the SARS-CoV-2 virus.

This special issue focuses on the role of SARS-CoV-2 in modifying the human immune response. In particular, we encourage authors to publish articles on the molecular mechanisms of virus action in the immune system. We are looking for articles on the immunomodulatory activity of SARS-CoV-2 in healthy people and patients suffering from various diseases related to the immune response, such as autoimmune diseases or cancer.

Dr. Katarzyna A. Lisowska
Guest Editor

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Keywords

  • SARS-CoV-2
  • COVID-19
  • immunomodulation
  • T cells
  • B cells
  • dendritic cells
  • monocytes
  • cytokines

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Published Papers (4 papers)

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Research

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18 pages, 24095 KiB  
Article
Genome-Wide Association Study of COVID-19 Breakthrough Infections and Genetic Overlap with Other Diseases: A Study of the UK Biobank
by Yaning Feng, Kenneth Chi-Yin Wong, Wai Kai Tsui, Ruoyu Zhang, Yong Xiang and Hon-Cheong So
Int. J. Mol. Sci. 2025, 26(13), 6441; https://doi.org/10.3390/ijms26136441 - 4 Jul 2025
Viewed by 256
Abstract
The coronavirus disease 2019 (COVID-19) pandemic has led to substantial health and financial burdens worldwide, and vaccines provide hope for reducing the burden of this pandemic. However, vaccinated people remain at risk for SARS-CoV-2 infection. Genome-wide association studies (GWASs) may identify potential genetic [...] Read more.
The coronavirus disease 2019 (COVID-19) pandemic has led to substantial health and financial burdens worldwide, and vaccines provide hope for reducing the burden of this pandemic. However, vaccinated people remain at risk for SARS-CoV-2 infection. Genome-wide association studies (GWASs) may identify potential genetic factors involved in the development of COVID-19 breakthrough infections (BIs); however, very few or no GWASs have been conducted for COVID-19 BI thus far. We conducted a GWAS and detailed bioinformatics analysis on COVID-19 BIs in a European population via the UK Biobank (UKBB). We conducted a series of analyses at different levels, including SNP-based, gene-based, pathway, and transcriptome-wide association analyses, to investigate genetic factors associated with COVID-19 BIs and hospitalized infections. The polygenic risk score (PRS) and Hoeffding’s test were performed to reveal the genetic relationships between BIs and other medical conditions. Two independent loci (LD-clumped at r2 = 0.01) reached genome-wide significance (p < 5 × 10−8), including rs36170929, which mapped to LOC102725191/VWDE, and rs28645263, which mapped to RETREG1. A pathway enrichment analysis highlighted pathways such as viral myocarditis, Rho-selective guanine exchange factor AKAP13 signaling, and lipid metabolism. The PRS analyses revealed significant genetic overlap between COVID-19 BIs and heart failure and between HbA1c and type 1 diabetes. Genetic dependence was also observed between COVID-19 BIs and asthma, lung abnormalities, schizophrenia, and type 1 diabetes on the basis of Hoeffding’s test. This GWAS revealed two significant loci that may be associated with COVID-19 BIs and a number of genes and pathways that may be involved in BIs. Genetic overlap with other diseases was identified. Further studies are warranted to replicate these findings and elucidate the mechanisms involved. Full article
(This article belongs to the Special Issue The Role of SARS-CoV-2 in Immunomodulation—Post-Pandemic Reflection on the Role of Viruses in Human Immunology)
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13 pages, 1921 KiB  
Article
Immune Modulation and Efficacy of Tixagevimab/Cilgavimab Pre-Exposure Prophylaxis in Lung Transplant Recipients During the Omicron Wave
by Lolita Sasset, Roberta Angioni, Nicolò Presa, Ricardo Sánchez-Rodríguez, Claudia Cozzolino, Nicole Bertoldi, Serena Marinello, Monica Loy, Maria Mazzitelli, Federico Rea, Annamaria Cattelan and Barbara Molon
Int. J. Mol. Sci. 2025, 26(8), 3696; https://doi.org/10.3390/ijms26083696 - 14 Apr 2025
Viewed by 382
Abstract
Lung transplant recipients are at increased risk of severe COVID-19 due to lifelong immunosuppressive therapy, which impairs both innate and adaptive immune responses. Identifying effective supportive therapies is essential for mitigating the heightened vulnerability of this population. This study investigated the effects of [...] Read more.
Lung transplant recipients are at increased risk of severe COVID-19 due to lifelong immunosuppressive therapy, which impairs both innate and adaptive immune responses. Identifying effective supportive therapies is essential for mitigating the heightened vulnerability of this population. This study investigated the effects of tixagevimab/cilgavimab, a monoclonal antibody therapy, as pre-exposure prophylaxis (PrEP) in this population. A prospective study was conducted on 19 lung transplant recipients at Padua University Hospital, Italy, during the Omicron variant wave (May–June 2022). Participants received tixagevimab/cilgavimab intramuscularly and were monitored for 180 days. SARS-CoV-2-specific antibody levels were measured at baseline (T0), one month (T1), and three months (T3) post-treatment. Cytokine profiles and clinical outcomes, including SARS-CoV-2 infections, were also assessed. At baseline, 50% of patients had negative antibody responses, but one-month post-treatment, all patients exceeded 700 kBAU/mL (median 3870 kBAU/mL), with levels decreasing but remaining positive at three months (median 1670 kBAU/mL). Remarkably, a higher level of circulating IL-18 was found at T3 in comparison to T0 in patients who did not experience COVID-19 after PrEP. This finding aligns with IL-18’s primary role in stimulating type-1 T helper (Th1) cell responses, necessary for the induction of virus-specific cytotoxic T lymphocytes (CTLs). These results suggest that tixagevimab/cilgavimab may induce a systemic immune signature that could contribute to priming the immune response against SARS-CoV-2, potentially mediated by interactions with immune cell subsets. Full article
(This article belongs to the Special Issue The Role of SARS-CoV-2 in Immunomodulation—Post-Pandemic Reflection on the Role of Viruses in Human Immunology)
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16 pages, 3479 KiB  
Article
Features of Highly Homologous T-Cell Receptor Repertoire in the Immune Response to Mutations in Immunogenic Epitopes
by Ksenia Zornikova, Dmitry Dianov, Natalia Ivanova, Vassa Davydova, Tatiana Nenasheva, Ekaterina Fefelova and Apollinariya Bogolyubova
Int. J. Mol. Sci. 2024, 25(23), 12591; https://doi.org/10.3390/ijms252312591 - 23 Nov 2024
Cited by 1 | Viewed by 1014
Abstract
CD8+ T-cell immunity, mediated through interactions between human leukocyte antigen (HLA) and the T-cell receptor (TCR), plays a pivotal role in conferring immune memory and protection against viral infections. The emergence of SARS-CoV-2 variants presents a significant challenge to the existing population immunity. [...] Read more.
CD8+ T-cell immunity, mediated through interactions between human leukocyte antigen (HLA) and the T-cell receptor (TCR), plays a pivotal role in conferring immune memory and protection against viral infections. The emergence of SARS-CoV-2 variants presents a significant challenge to the existing population immunity. While numerous SARS-CoV-2 mutations have been associated with immune evasion from CD8+ T cells, the molecular effects of most mutations on epitope-specific TCR recognition remain largely unexplored, particularly for epitope-specific repertoires characterized by common TCRs. In this study, we investigated an HLA-A*24-restricted NYN epitope (Spike448-456) that elicits broad and highly homologous CD8+ T cell responses in COVID-19 patients. Eleven naturally occurring mutations in the NYN epitope, all of which retained cell surface presentation by HLA, were tested against four transgenic Jurkat reporter cell lines. Our findings demonstrate that, with the exception of L452R and the combined mutation L452Q + Y453F, these mutations have minimal impact on the avidity of recognition by NYN peptide-specific TCRs. Additionally, we observed that a similar TCR responded differently to mutant epitopes and demonstrated cross-reactivity to the unrelated VYF epitope (ORF3a112-120). The results contradict the idea that immune responses with limited receptor diversity are insufficient to provide protection against emerging variants. Full article
(This article belongs to the Special Issue The Role of SARS-CoV-2 in Immunomodulation—Post-Pandemic Reflection on the Role of Viruses in Human Immunology)
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Review

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26 pages, 1044 KiB  
Review
Immunomodulatory Mechanisms Underlying Neurological Manifestations in Long COVID: Implications for Immune-Mediated Neurodegeneration
by Zaw Myo Hein, Thazin, Suresh Kumar, Muhammad Danial Che Ramli and Che Mohd Nasril Che Mohd Nassir
Int. J. Mol. Sci. 2025, 26(13), 6214; https://doi.org/10.3390/ijms26136214 - 27 Jun 2025
Viewed by 1214
Abstract
The COVID-19 pandemic has revealed the profound and lasting impact of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) on the nervous system. Beyond acute infection, SARS-CoV-2 acts as a potent immunomodulatory agent, disrupting immune homeostasis and contributing to persistent inflammation, autoimmunity, and neurodegeneration. [...] Read more.
The COVID-19 pandemic has revealed the profound and lasting impact of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) on the nervous system. Beyond acute infection, SARS-CoV-2 acts as a potent immunomodulatory agent, disrupting immune homeostasis and contributing to persistent inflammation, autoimmunity, and neurodegeneration. Long COVID, or post-acute sequelae of SARS-CoV-2 infection (PASC), is characterized by a spectrum of neurological symptoms, including cognitive dysfunction, fatigue, neuropathy, and mood disturbances. These are linked to immune dysregulation involving cytokine imbalance, blood–brain barrier (BBB) disruption, glial activation, and T-cell exhaustion. Key biomarkers such as interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), glial fibrillary acidic protein (GFAP), and neurofilament light chain (NFL) correlate with disease severity and chronicity. This narrative review examines the immunopathological mechanisms underpinning the neurological sequelae of long COVID, focusing on neuroinflammation, endothelial dysfunction, and molecular mimicry. We also assess the role of viral variants in shaping neuroimmune outcomes and explore emerging diagnostic and therapeutic strategies, including biomarker-guided and immune-targeted interventions. By delineating how SARS-CoV-2 reshapes neuroimmune interactions, this review aims to support the development of precision-based diagnostics and targeted therapies for long COVID-related neurological dysfunction. Emerging approaches include immune-modulatory agents (e.g., anti-IL-6), neuroprotective drugs, and strategies for repurposing antiviral or anti-inflammatory compounds in neuro-COVID. Given the high prevalence of comorbidities, personalized therapies guided by biomarkers and patient-specific immune profiles may be essential. Advancements in vaccine technologies and targeted biologics may also hold promise for prevention and disease modification. Finally, continued interdisciplinary research is needed to clarify the complex virus–immune–brain axis in long COVID and inform effective clinical management. Full article
(This article belongs to the Special Issue The Role of SARS-CoV-2 in Immunomodulation—Post-Pandemic Reflection on the Role of Viruses in Human Immunology)
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