The Role of Oxidative Stress in Viral Infections

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: closed (20 January 2023) | Viewed by 6110

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Guest Editor
Instituto de Investigación Sanitaria del Principado de Asturias (ISPA), Hospital Universitario Central de Asturias (HUCA), 33011 Oviedo, Spain
Interests: development of methods for detection quantification and genotyping of microorganisms of clinical interest for diagnostic purposes and study on the role of oxidative stress in various biological processes, especially in viral infections

Special Issue Information

Dear Colleagues:

The production of reactive oxygen species (ROS) occurs under normal physiological conditions and plays beneficial roles in important signaling pathways required for essential cellular functions.  Nevertheless, a redox imbalance is produced when systemic levels of ROS overwhelm the cellular antioxidant capacity, causing oxidative stress. This stress can be triggered by several situations, including viral infections, and causes the alteration of certain cellular mechanisms, such as the activation of endoplasmic reticulum stress and the triggering of the unfolded protein response, as well as the modulation of autophagy and/or apoptosis. These viral-induced responses facilitate viral replication and proliferation, enhancing viral pathogenesis. On the other hand, the innate immune system responds to viral infection by activating macrophage and dendritic cells, which contribute to inflammation. Oxidative stress and inflammation are closely related pathophysiological processes, one of which can be induced by another. Control of the immune-regulatory events is crucial in order to develop a protective immune response and to avoid the triggering of an exacerbated inflammatory response. The study of these oxidative and/or inflammatory pathways is essential in order to understand the cellular mechanisms involved in viral infection and open the possibility of developing drugs that block some of the described processes. In fact, several antioxidants (e.g., melatonin; vitamins A, C, and D; resveratrol) have been proposed as candidates to be part of the arsenal to treat—or at least attenuate—symptoms and sequelae caused by different viral infections.

Contributions to this Special Issue may cover all research aspects related to the implications of oxidative stress in viral pathogenesis and the therapeutic potential of antioxidants.

Dr. José Antonio Boga
Guest Editor

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Keywords

  • viral infection
  • oxidative stress
  • inflammation
  • endoplasmic reticulum stress
  • unfolded protein response
  • autophagy
  • apoptosis
  • antioxidants

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Published Papers (2 papers)

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Research

20 pages, 3295 KiB  
Article
Potential Role of Superoxide Dismutase 3 (SOD3) in Resistance to Influenza A Virus Infection
by Feimin Chen, Liurong Chen, Jinlong Liang, Zhixuan Chen, Chunyu Zhang, Zhengyin Zhang and Jie Yang
Antioxidants 2023, 12(2), 354; https://doi.org/10.3390/antiox12020354 - 2 Feb 2023
Cited by 5 | Viewed by 2572
Abstract
Influenza A virus infection induces the production of excessive reactive oxygen species (ROS). Overproduction of ROS can overwhelm the antioxidant defense system, leading to increasing intensive oxidative stress. However, antioxidant defense against oxidative damage induced by influenza A virus infection, and in particular [...] Read more.
Influenza A virus infection induces the production of excessive reactive oxygen species (ROS). Overproduction of ROS can overwhelm the antioxidant defense system, leading to increasing intensive oxidative stress. However, antioxidant defense against oxidative damage induced by influenza A virus infection, and in particular the significance of the SOD3 response in the pathogenesis of influenza virus infection, has not been well characterized. Here, we investigated the potential role of SOD3 in resistance to influenza A virus infection. In this study, SOD3, as an important antioxidant enzyme, was shown to be highly elevated in A549 cells following influenza A virus infection. Furthermore, inhibition of SOD3 impacted viral replication and virulence. We found that SOD3 disrupts IAV replication by impairing the synthesis of vRNA, whereas it did not affect viral ribonucleoprotein nuclear export. In addition, overexpression of SOD3 greatly reduced the levels of ROS caused by influenza A virus infection, regulated the inflammatory response to virus infection by inhibiting the phosphorylation of p65 of the NF-κB signaling pathway, and inhibited virus-induced apoptosis to a certain extent. Taken together, these findings indicate that SOD3 is actively involved in influenza A virus replication. Pharmacological modulation or targeting of SOD3 may pave the way for a novel therapeutic approach to combating influenza A virus infection. Full article
(This article belongs to the Special Issue The Role of Oxidative Stress in Viral Infections)
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16 pages, 6624 KiB  
Article
All-Trans Retinoic Acid Attenuates Transmissible Gastroenteritis Virus-Induced Apoptosis in IPEC-J2 Cells via Inhibiting ROS-Mediated P38MAPK Signaling Pathway
by Junning Pu, Daiwen Chen, Gang Tian, Jun He, Zhiqing Huang, Ping Zheng, Xiangbing Mao, Jie Yu, Junqiu Luo, Yuheng Luo, Hui Yan and Bing Yu
Antioxidants 2022, 11(2), 345; https://doi.org/10.3390/antiox11020345 - 10 Feb 2022
Cited by 12 | Viewed by 2578
Abstract
Transmissible gastroenteritis virus (TGEV) can cause diarrhea, dehydration, and high mortality in piglets, which is closely related to intestinal epithelial cell apoptosis caused by TGEV infection. All-trans retinoic acid (ATRA) is the active metabolite of vitamin A, which has antioxidant and anti-apoptotic properties. [...] Read more.
Transmissible gastroenteritis virus (TGEV) can cause diarrhea, dehydration, and high mortality in piglets, which is closely related to intestinal epithelial cell apoptosis caused by TGEV infection. All-trans retinoic acid (ATRA) is the active metabolite of vitamin A, which has antioxidant and anti-apoptotic properties. However, it is unknown whether ATRA can attenuate TGEV-induced IPEC-J2 cells apoptosis. Therefore, we investigated the protective effects of ATRA on TGEV-induced apoptosis of IPEC-J2 cells and explored the potential molecular mechanism. Our results indicated that TGEV infection caused IPEC-J2 cells damage and apoptosis. However, ATRA treatment attenuated TGEV-induced IPEC-J2 cells damage by upregulating the mRNA expressions of ZO-1, Occludin, and Mucin-1. ATRA treatment also attenuated TGEV-induced apoptosis in IPEC-J2 cells by downregulating the expression of Caspase-3, which is related to the inhibition of death receptor (Fas and Caspase-8) and mitochondrial (Bax, Bcl-2, and Caspase-9) pathways. Moreover, ATRA treatment prevented TGEV-induced ROS and MDA production and the upregulation of P38MAPK phosphorylation level, which is related to the increase in the activities of antioxidant enzymes (SOD, CAT, and T-AOC) and the mRNA abundance of antioxidant-related genes (GPX1, GPX2, SOD1, CAT, GCLC, and GCLM). In addition, treatment of TGEV-infected IPEC-J2 cells with the ROS inhibitors (NAC) significantly reduced the protein levels of p-P38MAPK, Fas, Bax, and Cleaved-caspase-3 and the percentage of apoptotic cells. Our results indicated that ATRA attenuated TGEV-induced apoptosis in IPEC-J2 cells via improving the antioxidant capacity, thereby inhibiting the cell damage. the mechanism of which is associated with the inhibition of ROS-mediated P38MAPK signaling pathway. Full article
(This article belongs to the Special Issue The Role of Oxidative Stress in Viral Infections)
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