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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 1740

Special Issue Editor


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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
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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 (2 papers)

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Research

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 182
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
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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 875
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
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