Immune Modulating Drugs in Viral Infections

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "Viral Immunology, Vaccines, and Antivirals".

Deadline for manuscript submissions: closed (30 September 2023) | Viewed by 1896

Special Issue Editor


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Guest Editor
1. College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea
2. Junglock Biomedical Institute, Daejeon, Republic of Korea
Interests: immunopathogenesis and etiological substances; early use of immune modulators (corticosteroids and other drugs) in viral infections
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Special Issue Information

Dear Colleagues,

At the present time, the pathophysiology of acute target-cell injury and a variety of clinical manifestations in viral infections, including COVID-19 and influenza, need to be further evaluated. During the COVID-19 pandemic, it was reported that immune-modulators, especially corticosteroids, reduce the morbidity and mortality of severely affected patients. Now, it is known that host immune systems react not only to pathogens but also to the substances originating from the pathogens, including toxins and pathogen-associated molecular patterns (PAMPs), and those originating from injured or infected host cells, including damage (danger)-associated molecular patterns (DAMPs), pathogenic proteins, and pathogenic peptides. In any viral infection, the host’s hyperactive or aberrant immune response to acute infectious insults, such as cytokine storm, may be related to host cell injury, and substances produced by injured target cells can induce even greater inflammation if they are released into the systemic circulation or local environment. Therefore, it is crucial to control initial hyperactive immune responses to reduce morbidity and prevent disease progression, and the early use of immune modulators such as corticosteroids, intravenous immunoglobulin and biologics has a basis for treating patients with acute severe viral infection. This Special Issue welcomes original or review articles and case reports related to any aspect of the use of immune-modulators for patients with viral infections, including COVID-19, and studies on pathogenesis, PAMPs, and DAMPs in viral infections.

Dr. Kyung-Yil Lee
Guest Editor

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Keywords

  • COVID-19
  • pathogenesis
  • immune modulators
  • corticosteroids
  • intravenous immunoglobulin
  • biologics
  • pathogen-associated molecular patterns (PAMPs)
  • damage (danger)-associated molecular patterns (DAMPs)

Published Papers (1 paper)

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Research

19 pages, 11762 KiB  
Article
Inhibitor of CD147 Suppresses T Cell Activation and Recruitment in CVB3-Induced Acute Viral Myocarditis
by Ruifang Wang, Kexin Zong, Juan Song, Qinqin Song, Dong Xia, Mi Liu, Haijun Du, Zhiqiang Xia, Hailan Yao and Jun Han
Viruses 2023, 15(5), 1137; https://doi.org/10.3390/v15051137 - 10 May 2023
Viewed by 1655
Abstract
Viral myocarditis (VMC) is a common disease characterized by cardiac inflammation. AC-73, an inhibitor of CD147, disrupts the dimerization of CD147, which participates in the regulation of inflammation. To explore whether AC-73 could alleviate cardiac inflammation induced by CVB3, mice were injected intraperitoneally [...] Read more.
Viral myocarditis (VMC) is a common disease characterized by cardiac inflammation. AC-73, an inhibitor of CD147, disrupts the dimerization of CD147, which participates in the regulation of inflammation. To explore whether AC-73 could alleviate cardiac inflammation induced by CVB3, mice were injected intraperitoneally with AC-73 on the fourth day post-infection (dpi) and sacrificed on the seventh dpi. Pathological changes in the myocardium, T cell activation or differentiation, and expression of cytokines were analyzed using H&E staining, flow cytometry, fluorescence staining and multiplex immunoassay. The results showed that AC-73 alleviated cardiac pathological injury and downregulated the percentage of CD45+CD3+ T cells in the CVB3-infected mice. The administration of AC-73 reduced the percentage of activated CD4+ and CD8+ T cells (CD69+ and/or CD38+) in the spleen, while the percentage of CD4+ T cell subsets in the spleen was not changed in the CVB3-infected mice. In addition, the infiltration of activated T cells (CD69+) and macrophages (F4/80+) in the myocardium also decreased after the AC-73 treatment. The results also showed that AC-73 inhibited the release of many cytokines and chemokines in the plasma of the CVB3-infected mice. In conclusion, AC-73 mitigated CVB3-induced myocarditis by inhibiting the activation of T cells and the recruitment of immune cells to the heart. Thus, CD147 may be a therapeutic target for virus-induced cardiac inflammation. Full article
(This article belongs to the Special Issue Immune Modulating Drugs in Viral Infections)
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