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      Glucose-6-Phosphate Dehydrogenase Deficiency Enhances Human Coronavirus 229E Infection

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          Abstract

          The host cellular environment is a key determinant of pathogen infectivity. Viral gene expression and viral particle production of glucose-6-phosphate dehydrogenase (G6PD)–deficient and G6PD-knockdown cells were much higher than their counterparts when human coronavirus (HCoV) 229E was applied at 0.1 multiplicity of infection. These phenomena were correlated with increased oxidant production. Accordingly, ectopic expression of G6PD in G6PD-deficient cells or addition of antioxidant (such as α-lipoic acid) to G6PD-knockdown cells attenuated the increased susceptibility to HCoV 229E infection. All experimental data indicated that oxidative stress in host cells is an important factor in HCoV 229E infectivity

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          Glucose-6-phosphate dehydrogenase--from oxidative stress to cellular functions and degenerative diseases.

          Daniel Tsun-Yee Chiu, Mei Cheng, Hung-Yao Ho (2006)
          Glucose-6-phosphate dehydrogenase (G6PD), the first and rate-limiting enzyme of the pentose phosphate pathway, is indispensable to maintenance of the cytosolic pool of NADPH and thus the cellular redox balance. The role of G6PD as an antioxidant enzyme has been recognized in erythrocytes for a long time, as its deficiency is associated with neonatal jaundice, drug- or infection-mediated hemolytic crisis, favism and, less commonly, chronic non-spherocytic hemolytic anemia. To a large extent, advances in the field were made on the pathophysiology of G6PD-deficient erythrocytes, and the molecular characterization of different G6PD variants. Not until recently did numerous studies cast light on the importance of G6PD in other aspects of the physiology of both cells and organisms. Deficiency in G6PD activity, and hence a disturbance in redox homeostasis, can lead to dysregulation of cell growth and signaling, anomalous embryonic development, altered susceptibility to viral infection as well as increased susceptibility to degenerative diseases. The present review covers recent developments in this field. Additionally, molecular characterization of G6PD variants, especially those frequently found in Taiwan and Southern China, is also addressed.
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            Reactive oxygen signaling and MAPK activation distinguish Epstein-Barr Virus (EBV)-positive versus EBV-negative Burkitt's lymphoma.

            Francesca Cerimele, Traci E. Battle, Rebecca Lynch … (2005)
            Burkitt's lymphoma (BL) is an aggressive B cell neoplasm, which is one of the most common neoplasms of childhood. It is highly widespread in East Africa, where it appears in endemic form associated with Epstein-Barr virus (EBV) infection, and around the world in a sporadic form in which EBV infection is much less common. In addition to being the first human neoplasm to be associated with EBV, BL is associated with a characteristic translocation, in which the Ig promoter is translocated to constitutively activate the c-myc oncogene. Although many BLs respond well to chemotherapy, a significant fraction fails to respond to therapy, leading to death. In this article, we demonstrate that EBV-positive BL expresses high levels of activated mitogen-activated protein kinase and reactive oxygen species (ROS), and that ROS directly regulate NF-kappaB activation. EBV-negative BLs exhibit activation of phosphoinositol 3-kinase, but do not have elevated levels of ROS. Elevated reactive oxygen may play a role in diverse forms of viral carcinogenesis in humans, including cancers caused by EBV, hepatitis B, C, and human T cell lymphotropic virus. Our findings imply that inhibition of ROS may be useful in the treatment of EBV-induced neoplasia.
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              Enhanced oxidative stress and accelerated cellular senescence in glucose-6-phosphate dehydrogenase (G6PD)-deficient human fibroblasts.

              Jenny Chiu, Edward A. Stern, Andy H Y Ho … (2000)
              Glucose-6-phosphate dehydrogenase (G6PD) is involved in the generation of reduced nicotinamide adenine dinucleotide phosphate (NADPH) and the maintenance of the cellular redox balance. The biological effects of G6PD deficiency in nucleated cells were studied using G6PD-deficient human foreskin fibroblasts (HFF). In contrast to that of normal HFF, the doubling time of G6PD-deficient cells increased readily from population doubling level (PDL) 15 to 63. This was accompanied by a significant increase in the percentage of G(1) cells. The slow-down in growth preceded an early entry of these cells into a nondividing state reminiscent of cellular senescence. These cells exhibited a significant increase in level of senescence-associated beta-galactosidase (SA-beta-gal) staining. The importance of G6PD activity in cell growth was corroborated by the finding that ectopic expression of active G6PD in the deficient cells prevented their growth retardation and early onset of senescence. Mechanistically, the enhanced fluorescence in dichlorofluorescin (H(2)DCF)-stained G6PD-deficient cells suggests the possible involvement of reactive oxygen species in senescence. Taken together, our results show that G6PD deficiency predisposes human fibroblasts to retarded growth and accelerated cellular senescence. Moreover, G6PD-deficient HFF provides a useful model system for delineating the effects of redox alterations on cellular processes.
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Infect Dis
                Journal ID (iso-abbrev): J. Infect. Dis
                Journal ID (hwp): jinfdis
                Journal ID (publisher-id): jid
                Title: The Journal of Infectious Diseases
                Publisher: The University of Chicago Press
                ISSN (Print): 0022-1899
                ISSN (Electronic): 1537-6613
                Publication date (Print): 15 March 2008
                Publication date (Electronic): 15 March 2008
                Publication date PMC-release: 15 March 2008
                Volume: 197
                Issue: 6
                Pages: 812-816
                Affiliations
                [1 ] Graduate Institute of Basic Medical Sciences and Graduate Institute of Medical Biotechnology, Chang Gung University, and Department of Clinical Pathology, Chang Gung Memorial Hospital Kwei-Shan, Tao-Yuan, Taiwan
                [2 ] Graduate Institute of Medical Biotechnology, Chang Gung University, and Department of Clinical Pathology, Chang Gung Memorial Hospital Kwei-Shan, Tao-Yuan, Taiwan
                [3 ] Department of Clinical Pathology, Chang Gung Memorial Hospital Kwei-Shan, Tao-Yuan, Taiwan
                Author notes
                Reprints or correspondence: Dr. Shin-Ru Shih, Graduate Institute of Basic Medical Sciences, Chang Gung University, 259 Wen-Hwa First Rd., Kwei-Shan, Tao-Yuan, Taiwan ( srshih@ 123456mail.cgu.edu.tw ) (for correspondence on virology); or, Dr. Daniel Tsun-Yee Chiu, Graduate Institute of Basic Medical Sciences, Chang Gung University, 259 Wen-Hwa First Rd., Kwei-Shan, Tao-Yuan, Taiwan ( dtychiu@ 123456mail.cgu.edu.tw ) (for reprints and all other correspondence)
                Article
                DOI: 10.1086/528377
                PMC ID: 7199897
                PubMed ID: 18269318
                SO-VID: d9d67d2c-3dab-4815-ae70-0194e04b1c41
                Copyright © © 2008 by the Infectious Diseases Society of America
                License:

                This article is made available via the PMC Open Access Subset for unrestricted re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the COVID-19 pandemic or until permissions are revoked in writing. Upon expiration of these permissions, PMC is granted a perpetual license to make this article available via PMC and Europe PMC, consistent with existing copyright protections.

                History
                Date received : 2 July 2007
                Date accepted : 1 October 2007
                Categories
                Subject: Major Articles And Brief Reports
                Subject: Viruses
                Subject: Brief Reports

                ScienceOpen disciplines: Infectious disease & Microbiology
                Data availability:
                ScienceOpen disciplines: Infectious disease & Microbiology

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