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Viruses
Special Issues
Role of Mitochondria in Viral Pathogenesis
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Role of Mitochondria in Viral Pathogenesis

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "General Virology".

Deadline for manuscript submissions: closed (30 September 2023) | Viewed by 9297

Special Issue Editors

Dr. Mohsin Khan

E-Mail Website
Guest Editor
Liver Disease Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institute of Health, Bethesda, MD 20814, USA
Interests: hepatitis B virus (HBV) pathogenesis; host-HBV interplay; antiviral drug discovery
Dr. Seong-Jun Kim

E-Mail Website
Guest Editor
Department of Convergent Research of Emerging Virus Infection, Korea Research Institute of Chemical Technology, Daejeon 34114, Korea
Interests: immunology; cell biology; Western blot analysis; RNA; gene expression; infection
Prof. Dr. Aleem Siddiqui

E-Mail Website
Guest Editor
Division of Infectious Diseases and Global Public Health, University of California, San Diego, La Jolla, CA 92093, USA
Interests: HBV; gene expression; innate immunity; DNA synthesis and transcription

Special Issue Information

Dear Colleagues,

Successful invasion and efficient multiplication often require the virus to hijack cellular machinery. This hijacking becomes more efficient if viruses can take over any cellular event (or organelle) that is responsible for multiple functions. Mitochondria, the powerhouse of the cell, are bioenergetic and biosynthetic organelles that perform multiple signaling and metabolic events. Collectively, these mitochondrial events are responsible for regulating cell survival, energy production, innate immune signaling, and apoptosis. In recent decades, although we have collectively made significant progress in uncovering the role of mitochondria in viral pathogenesis, there are many issues that still need attention and can be crucial to fully understand viral–mitochondria interplay.

We are excited to announce that we will be compiling a new Special Issue entitled ‘Role of Mitochondria in Viral Pathogenesis’, to be published in the journal Viruses. Viruses is an open access journal that provides a platform for the studies of viruses. Here, we encourage our fellow scientists to share their experimental and/or theoretical results within the scope of the above title in the form of original research or review articles. This Special Issue aims to cover DNA and RNA viruses of human and animal host ranges. Broadly, blood-borne, zoonotic, emerging, and newly identified viruses (or viral strains) are highly relevant to this Special Issue. The relevant research areas include (but are not limited to) the following:

  • Mitochondrial dynamics and its role in viral infection;
  • Hijacking of mitochondrial signaling to manipulate cell survival, death, proliferation;
  • Involvement of mitochondria in the pathogenesis of viruses such as HBV, HCV, HIV, Zika, Dengue, HIV, KSHV, influenza viruses, SARS CoV2, MERS, Ebola, etc.;
  • Role of mitochondria in antiviral signaling and interferon production;
  • Mitochondrial crosstalk with other cellular organelles and its implications in viral infection;
  • Viral metabolomics;
  • Mitochondrial oxidative phosphorylation.

We look forward to receiving your contributions.

Dr. Mohsin Khan
Dr. Seong-Jun Kim
Prof. Dr. Aleem Siddiqui
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Viruses is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • mitochondrial dynamics
  • innate immunity
  • mitochondrial antiviral signaling protein (MAVS)
  • mitophagy
  • apoptosis
  • oxidative phosphorylation
  • oxidative stress
  • parkin translocation
  • lysosomal degradation
  • interferon signaling
  • inflammasome dynamics
  • mitochondrial bioenergetics
  • alteration in mitochondrial membrane potential

Published Papers (6 papers)

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Research

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21 pages, 4566 KiB  
Article
Ultrastructural and Functional Characterization of Mitochondrial Dynamics Induced by Human Respiratory Syncytial Virus Infection in HEp-2 Cells
by Ignacio Lara-Hernandez, Juan Carlos Muñoz-Escalante, Sofía Bernal-Silva, Daniel E. Noyola, Rosa María Wong-Chew, Andreu Comas-García and Mauricio Comas-Garcia
Viruses 2023, 15(7), 1518; https://doi.org/10.3390/v15071518 - 07 Jul 2023
Cited by 1 | Viewed by 1498
Abstract
Human respiratory syncytial virus (hRSV) is the leading cause of acute lower respiratory tract infections in children under five years of age and older adults worldwide. During hRSV infection, host cells undergo changes in endomembrane organelles, including mitochondria. This organelle is responsible for [...] Read more.
Human respiratory syncytial virus (hRSV) is the leading cause of acute lower respiratory tract infections in children under five years of age and older adults worldwide. During hRSV infection, host cells undergo changes in endomembrane organelles, including mitochondria. This organelle is responsible for energy production in the cell and plays an important role in the antiviral response. The present study focuses on characterizing the ultrastructural and functional changes during hRSV infection using thin-section transmission electron microscopy and RT-qPCR. Here we report that hRSV infection alters mitochondrial morphodynamics by regulating the expression of key genes in the antiviral response process, such as Mfn1, VDAC2, and PINK1. Our results suggest that hRSV alters mitochondrial morphology during infection, producing a mitochondrial phenotype with shortened cristae, swollen matrix, and damaged membrane. We also observed that hRSV infection modulates the expression of the aforementioned genes, possibly as an evasion mechanism in the face of cellular antiviral response. Taken together, these results advance our knowledge of the ultrastructural alterations associated with hRSV infection and might guide future therapeutic efforts to develop effective antiviral drugs for hRSV treatment. Full article
(This article belongs to the Special Issue Role of Mitochondria in Viral Pathogenesis)
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16 pages, 4764 KiB  
Article
Microplitis bicoloratus Bracovirus Promotes Cyclophilin D-Acetylation at Lysine 125 That Correlates with Apoptosis during Insect Immunosuppression
by Dan Yu, Pan Zhang, Cuixian Xu, Yan Hu, Yaping Liang and Ming Li
Viruses 2023, 15(7), 1491; https://doi.org/10.3390/v15071491 - 30 Jun 2023
Viewed by 881
Abstract
Cyclophilin D (CypD) is regulated during the innate immune response of insects. However, the mechanism by which CypD is activated under innate immunosuppression is not understood. Microplitis bicoloratus bracovirus (MbBV), a symbiotic virus in the parasitoid wasp, Microplitis bicoloratus, suppresses innate immunity [...] Read more.
Cyclophilin D (CypD) is regulated during the innate immune response of insects. However, the mechanism by which CypD is activated under innate immunosuppression is not understood. Microplitis bicoloratus bracovirus (MbBV), a symbiotic virus in the parasitoid wasp, Microplitis bicoloratus, suppresses innate immunity in parasitized Spodoptera litura. Here, we demonstrate that MbBV promotes the CypD acetylation of S. litura, resulting in an immunosuppressive phenotype characterized by increased apoptosis of hemocytes and MbBV-infected cells. Under MbBV infection, the inhibition of CypD acetylation significantly rescued the apoptotic cells induced by MbBV, and the point-mutant fusion proteins of CypDK125R-V5 were deacetylated. The CypD-V5 fusion proteins were acetylated in MbBV-infected cells. Deacetylation of CypDK125R-V5 can also suppress the MbBV-induced increase in apoptosis. These results indicate that CypD is involved in the MbBV-suppressed innate immune response via the CypD-acetylation pathway and S. litura CypD is acetylated on K125. Full article
(This article belongs to the Special Issue Role of Mitochondria in Viral Pathogenesis)
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16 pages, 1612 KiB  
Article
Effect of Vaccination on Platelet Mitochondrial Bioenergy Function of Patients with Post-Acute COVID-19
by Anna Gvozdjáková, Jarmila Kucharská, Zuzana Rausová, Guillermo Lopéz-Lluch, Plácido Navas, Patrik Palacka, Barbora Bartolčičová and Zuzana Sumbalová
Viruses 2023, 15(5), 1085; https://doi.org/10.3390/v15051085 - 28 Apr 2023
Viewed by 1563
Abstract
Background: Mitochondrial dysfunction and redox cellular imbalance indicate crucial function in COVID-19 pathogenesis. Since 11 March 2020, a global pandemic, health crisis and economic disruption has been caused by SARS-CoV-2 virus. Vaccination is considered one of the most effective strategies for preventing viral [...] Read more.
Background: Mitochondrial dysfunction and redox cellular imbalance indicate crucial function in COVID-19 pathogenesis. Since 11 March 2020, a global pandemic, health crisis and economic disruption has been caused by SARS-CoV-2 virus. Vaccination is considered one of the most effective strategies for preventing viral infection. We tested the hypothesis that preventive vaccination affects the reduced bioenergetics of platelet mitochondria and the biosynthesis of endogenous coenzyme Q10 (CoQ10) in patients with post-acute COVID-19. Material and Methods: 10 vaccinated patients with post-acute COVID-19 (V + PAC19) and 10 unvaccinated patients with post-acute COVID-19 (PAC19) were included in the study. The control group (C) consisted of 16 healthy volunteers. Platelet mitochondrial bioenergy function was determined with HRR method. CoQ10, γ-tocopherol, α-tocopherol and β-carotene were determined by HPLC, TBARS (thiobarbituric acid reactive substances) were determined spectrophotometrically. Results: Vaccination protected platelet mitochondrial bioenergy function but not endogenous CoQ10 levels, in patients with post-acute COVID-19. Conclusions: Vaccination against SARS-CoV-2 virus infection prevented the reduction of platelet mitochondrial respiration and energy production. The mechanism of suppression of CoQ10 levels by SARS-CoV-2 virus is not fully known. Methods for the determination of CoQ10 and HRR can be used for monitoring of mitochondrial bioenergetics and targeted therapy of patients with post-acute COVID-19. Full article
(This article belongs to the Special Issue Role of Mitochondria in Viral Pathogenesis)
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18 pages, 1455 KiB  
Article
ROS-Induced Mitochondrial Dysfunction in CD4 T Cells from ART-Controlled People Living with HIV
by Madison Schank, Juan Zhao, Ling Wang, Lam Ngoc Thao Nguyen, Yi Zhang, Xiao Y. Wu, Jinyu Zhang, Yong Jiang, Shunbin Ning, Mohamed El Gazzar, Jonathan P. Moorman and Zhi Q. Yao
Viruses 2023, 15(5), 1061; https://doi.org/10.3390/v15051061 - 26 Apr 2023
Cited by 7 | Viewed by 1663
Abstract
We have previously demonstrated mitochondrial dysfunction in aging CD4 T cells from antiretroviral therapy (ART)-controlled people living with HIV (PLWH). However, the underlying mechanisms by which CD4 T cells develop mitochondrial dysfunction in PLWH remain unclear. In this study, we sought to elucidate [...] Read more.
We have previously demonstrated mitochondrial dysfunction in aging CD4 T cells from antiretroviral therapy (ART)-controlled people living with HIV (PLWH). However, the underlying mechanisms by which CD4 T cells develop mitochondrial dysfunction in PLWH remain unclear. In this study, we sought to elucidate the mechanism(s) of CD4 T cell mitochondrial compromise in ART-controlled PLWH. We first assessed the levels of reactive oxygen species (ROS), and we observed significantly increased cellular and mitochondrial ROS levels in CD4 T cells from PLWH compared to healthy subjects (HS). Furthermore, we observed a significant reduction in the levels of proteins responsible for antioxidant defense (superoxide dismutase 1, SOD1) and ROS-mediated DNA damage repair (apurinic/apyrimidinic endonuclease 1, APE1) in CD4 T cells from PLWH. Importantly, CRISPR/Cas9-mediated knockdown of SOD1 or APE1 in CD4 T cells from HS confirmed their roles in maintaining normal mitochondrial respiration via a p53-mediated pathway. Reconstitution of SOD1 or APE1 in CD4 T cells from PLWH successfully rescued mitochondrial function as evidenced by Seahorse analysis. These results indicate that ROS induces mitochondrial dysfunction, leading to premature T cell aging via dysregulation of SOD1 and APE1 during latent HIV infection. Full article
(This article belongs to the Special Issue Role of Mitochondria in Viral Pathogenesis)
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Review

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19 pages, 4337 KiB  
Review
Mitochondrial Oxidative Phosphorylation in Viral Infections
by Neeraja Purandare, Esha Ghosalkar, Lawrence I. Grossman and Siddhesh Aras
Viruses 2023, 15(12), 2380; https://doi.org/10.3390/v15122380 - 04 Dec 2023
Viewed by 1756
Abstract
Mitochondria have been identified as the “powerhouse” of the cell, generating the cellular energy, ATP, for almost seven decades. Research over time has uncovered a multifaceted role of the mitochondrion in processes such as cellular stress signaling, generating precursor molecules, immune response, and [...] Read more.
Mitochondria have been identified as the “powerhouse” of the cell, generating the cellular energy, ATP, for almost seven decades. Research over time has uncovered a multifaceted role of the mitochondrion in processes such as cellular stress signaling, generating precursor molecules, immune response, and apoptosis to name a few. Dysfunctional mitochondria resulting from a departure in homeostasis results in cellular degeneration. Viruses hijack host cell machinery to facilitate their own replication in the absence of a bonafide replication machinery. Replication being an energy intensive process necessitates regulation of the host cell oxidative phosphorylation occurring at the electron transport chain in the mitochondria to generate energy. Mitochondria, therefore, can be an attractive therapeutic target by limiting energy for viral replication. In this review we focus on the physiology of oxidative phosphorylation and on the limited studies highlighting the regulatory effects viruses induce on the electron transport chain. Full article
(This article belongs to the Special Issue Role of Mitochondria in Viral Pathogenesis)
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12 pages, 2126 KiB  
Review
Regulation of Mitochondrial Metabolism by Hepatitis B Virus
by Yumei Li and Jing-hsiung James Ou
Viruses 2023, 15(12), 2359; https://doi.org/10.3390/v15122359 - 30 Nov 2023
Cited by 1 | Viewed by 1293
Abstract
Mitochondria play important roles in the synthesis of ATP, the production of reactive oxygen species, and the regulation of innate immune response and apoptosis. Many viruses perturb mitochondrial activities to promote their replication and cause cell damage. Hepatitis B virus (HBV) is a [...] Read more.
Mitochondria play important roles in the synthesis of ATP, the production of reactive oxygen species, and the regulation of innate immune response and apoptosis. Many viruses perturb mitochondrial activities to promote their replication and cause cell damage. Hepatitis B virus (HBV) is a hepatotropic virus that can cause severe liver diseases, including cirrhosis and hepatocellular carcinoma (HCC). This virus can also alter mitochondrial functions and metabolism to promote its replication and persistence. In this report, we summarize recent research progress on the interaction between HBV and mitochondrial metabolism, as well as the effect this interaction has on HBV replication and persistence. Full article
(This article belongs to the Special Issue Role of Mitochondria in Viral Pathogenesis)
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