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      Redox Biology of Respiratory Viral Infections

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          Abstract

          Respiratory viruses cause infections of the upper or lower respiratory tract and they are responsible for the common cold—the most prevalent disease in the world. In many cases the common cold results in severe illness due to complications, such as fever or pneumonia. Children, old people, and immunosuppressed patients are at the highest risk and require fast diagnosis and therapeutic intervention. However, the availability and efficiencies of existing therapeutic approaches vary depending on the virus. Investigation of the pathologies that are associated with infection by respiratory viruses will be paramount for diagnosis, treatment modalities, and the development of new therapies. Changes in redox homeostasis in infected cells are one of the key events that is linked to infection with respiratory viruses and linked to inflammation and subsequent tissue damage. Our review summarizes current knowledge on changes to redox homeostasis, as induced by the different respiratory viruses.

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          The Nrf2-antioxidant response element signaling pathway and its activation by oxidative stress.

          Truyen Nguyen, Paul Nioi, Cecil B. Pickett (2009)
          A major mechanism in the cellular defense against oxidative or electrophilic stress is activation of the Nrf2-antioxidant response element signaling pathway, which controls the expression of genes whose protein products are involved in the detoxication and elimination of reactive oxidants and electrophilic agents through conjugative reactions and by enhancing cellular antioxidant capacity. At the molecular level, however, the regulatory mechanisms involved in mediating Nrf2 activation are not fully understood. It is well established that Nrf2 activity is controlled, in part, by the cytosolic protein Keap1, but the nature of this pathway and the mechanisms by which Keap1 acts to repress Nrf2 activity remain to be fully characterized and are the topics of discussion in this minireview. In addition, a possible role of the Nrf2-antioxidant response element transcriptional pathway in neuroprotection will also be discussed.
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            Superoxide dismutases: role in redox signaling, vascular function, and diseases.

            Tohru Fukai, Masuko Ushio-Fukai (2011)
            Excessive reactive oxygen species Revised abstract, especially superoxide anion (O₂•-), play important roles in the pathogenesis of many cardiovascular diseases, including hypertension and atherosclerosis. Superoxide dismutases (SODs) are the major antioxidant defense systems against (O₂•-), which consist of three isoforms of SOD in mammals: the cytoplasmic Cu/ZnSOD (SOD1), the mitochondrial MnSOD (SOD2), and the extracellular Cu/ZnSOD (SOD3), all of which require catalytic metal (Cu or Mn) for their activation. Recent evidence suggests that in each subcellular location, SODs catalyze the conversion of (O₂•-), H2O2, which may participate in cell signaling. In addition, SODs play a critical role in inhibiting oxidative inactivation of nitric oxide, thereby preventing peroxynitrite formation and endothelial and mitochondrial dysfunction. The importance of each SOD isoform is further illustrated by studies from the use of genetically altered mice and viral-mediated gene transfer. Given the essential role of SODs in cardiovascular disease, the concept of antioxidant therapies, that is, reinforcement of endogenous antioxidant defenses to more effectively protect against oxidative stress, is of substantial interest. However, the clinical evidence remains controversial. In this review, we will update the role of each SOD in vascular biologies, physiologies, and pathophysiologies such as atherosclerosis, hypertension, and angiogenesis. Because of the importance of metal cofactors in the activity of SODs, we will also discuss how each SOD obtains catalytic metal in the active sites. Finally, we will discuss the development of future SOD-dependent therapeutic strategies.
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              Human rhinoviruses.

              Samantha E Jacobs, Daryl M. Lamson, Kirsten St. George … (2013)
              Human rhinoviruses (HRVs), first discovered in the 1950s, are responsible for more than one-half of cold-like illnesses and cost billions of dollars annually in medical visits and missed days of work. Advances in molecular methods have enhanced our understanding of the genomic structure of HRV and have led to the characterization of three genetically distinct HRV groups, designated groups A, B, and C, within the genus Enterovirus and the family Picornaviridae. HRVs are traditionally associated with upper respiratory tract infection, otitis media, and sinusitis. In recent years, the increasing implementation of PCR assays for respiratory virus detection in clinical laboratories has facilitated the recognition of HRV as a lower respiratory tract pathogen, particularly in patients with asthma, infants, elderly patients, and immunocompromised hosts. Cultured isolates of HRV remain important for studies of viral characteristics and disease pathogenesis. Indeed, whether the clinical manifestations of HRV are related directly to viral pathogenicity or secondary to the host immune response is the subject of ongoing research. There are currently no approved antiviral therapies for HRVs, and treatment remains primarily supportive. This review provides a comprehensive, up-to-date assessment of the basic virology, pathogenesis, clinical epidemiology, and laboratory features of and treatment and prevention strategies for HRVs.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Viruses
                Journal ID (iso-abbrev): Viruses
                Journal ID (publisher-id): viruses
                Title: Viruses
                Publisher: MDPI
                ISSN (Electronic): 1999-4915
                Publication date (Electronic): 26 July 2018
                Publication date Collection: August 2018
                Volume: 10
                Issue: 8
                Electronic Location Identifier: 392
                Affiliations
                [1 ]Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, Vavilov str, 32, 119991 Moscow, Russia; kochet@ 123456eimb.ru
                [2 ]Inserm U1052, Cancer Research Center Lyon, University of Lyon, 69000 Lyon, France; birke.bartosch@ 123456inserm.fr
                [3 ]DevWeCan Laboratories of Excellence Network (Labex), 69003 Lyon, France
                Author notes
                [* ]Correspondence: o.a.khomich@ 123456gmail.com (O.A.K.); aivanov@ 123456yandex.ru or aivanov@ 123456eimb.ru (A.V.I.); Tel.: +7-499-135-6065 (A.V.I.)
                Author information
                https://orcid.org/0000-0001-6354-4660
                https://orcid.org/0000-0002-5659-9679
                Article
                Publisher ID: viruses-10-00392
                DOI: 10.3390/v10080392
                PMC ID: 6115776
                PubMed ID: 30049972
                SO-VID: 3a8a8c7f-9df5-420f-a2a9-844e2fd5ced4
                Copyright © © 2018 by the authors.
                License:

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 13 June 2018
                Date accepted : 24 July 2018
                Categories
                Subject: Review

                ScienceOpen disciplines: Microbiology & Virology
                Keywords: oxidative stress,reactive oxygen species,influenza virus,respiratory syncytial virus,rhinovirus,nrf2,inflammation
                Data availability:
                ScienceOpen disciplines: Microbiology & Virology
                Keywords: oxidative stress, reactive oxygen species, influenza virus, respiratory syncytial virus, rhinovirus, nrf2, inflammation

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