Mitochondria-mediated oxidative stress during viral infection

Foo, J.T.W.; Bellot, Gaëtan; Pervaiz, Shazib; Alonso, Sylvie

doi:10.1016/j.tim.2021.12.011

Cited by 131 publications

(125 citation statements)

References 111 publications

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“…An additional mitochondrial function disrupted during viral infections is the production of ROS. Viral infections cause increased cellular ROS through mitochondrial deregulation [ 163 ]. Viruses depolarize the mitochondrial transmembrane potential (MMP), which contributes to the accumulation of ROS.…”

Section: Viruses and Mitochondrial Changes And Tca Cycle Rewiringmentioning

confidence: 99%

Hallmarks of Metabolic Reprogramming and Their Role in Viral Pathogenesis

Allen

Arjona

Santerre

et al. 2022

Viruses

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Metabolic reprogramming is a hallmark of cancer and has proven to be critical in viral infections. Metabolic reprogramming provides the cell with energy and biomass for large-scale biosynthesis. Based on studies of the cellular changes that contribute to metabolic reprogramming, seven main hallmarks can be identified: (1) increased glycolysis and lactic acid, (2) increased glutaminolysis, (3) increased pentose phosphate pathway, (4) mitochondrial changes, (5) increased lipid metabolism, (6) changes in amino acid metabolism, and (7) changes in other biosynthetic and bioenergetic pathways. Viruses depend on metabolic reprogramming to increase biomass to fuel viral genome replication and production of new virions. Viruses take advantage of the non-metabolic effects of metabolic reprogramming, creating an anti-apoptotic environment and evading the immune system. Other non-metabolic effects can negatively affect cellular function. Understanding the role metabolic reprogramming plays in viral pathogenesis may provide better therapeutic targets for antivirals.

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Section: Viruses and Mitochondrial Changes And Tca Cycle Rewiringmentioning

confidence: 99%

Hallmarks of Metabolic Reprogramming and Their Role in Viral Pathogenesis

Allen

Arjona

Santerre

et al. 2022

Viruses

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“…Mitochondrial PHBs have an important role in stabilizing the dynamin-related OPA1, a protein that promotes mitochondrial fusion ( Merkwirth et al., 2007 ; Ban et al., 2017 ). These PHBs also contribute to the electron chain transport activity, to maintain the integrity of the mitochondrial inner membrane ( Foo et al., 2021 ). Furthermore, previous studies on arboviruses have identified surface PHB as a receptor for DENV entrance in Ae.…”

Section: Discussionmentioning

confidence: 99%

“…While DENV and ZIKV also manipulate host autophagy to improve their replication levels ( Datan et al., 2016 ), apoptotic blebs containing CHIKV particles have been observed ( Joubert et al., 2012 ). Furthermore, proteins of viruses such as HCV and HIV have been shown to interact with host mitochondrial membranes to increase ROS production and benefit viral replication ( Foo et al., 2021 ).…”

Section: Discussionmentioning

confidence: 99%

“…Two significant cell sites for ROS production are the mitochondrial Complexes I and III of the electron transport chain ( Chen et al., 2003 ; Foo et al., 2021 ). In the present study, the Aag-2 Rieske subunit of the ubiquinol-cytochrome b-c1 reductase (CIII) mitochondrial complex (Q17EQ1, FC 48 hpi vs. Control +0.43, Cluster 2) was more abundant at 48 hpi rather than at 12 hpi and Control.…”

Section: Discussionmentioning

confidence: 99%

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Aedes aegypti Aag-2 Cell Proteome Modulation in Response to Chikungunya Virus Infection

Vasconcellos

Melo

Mandacaru

et al. 2022

Front. Cell. Infect. Microbiol.

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Chikungunya virus (CHIKV) is a single-stranded positive RNA virus that belongs to the genus Alphavirus and is transmitted to humans by infected Aedes aegypti and Aedes albopictus bites. In humans, CHIKV usually causes painful symptoms during acute and chronic stages of infection. Conversely, virus–vector interaction does not disturb the mosquito’s fitness, allowing a persistent infection. Herein, we studied CHIKV infection of Ae. aegypti Aag-2 cells (multiplicity of infection (MOI) of 0.1) for 48 h through label-free quantitative proteomic analysis and transmission electron microscopy (TEM). TEM images showed a high load of intracellular viral cargo at 48 h postinfection (hpi), as well as an unusual elongated mitochondria morphology that might indicate a mitochondrial imbalance. Proteome analysis revealed 196 regulated protein groups upon infection, which are related to protein synthesis, energy metabolism, signaling pathways, and apoptosis. These Aag-2 proteins regulated during CHIKV infection might have roles in antiviral and/or proviral mechanisms and the balance between viral propagation and the survival of host cells, possibly leading to the persistent infection.

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“…However, excessive ROS production can be as damaging as coronavirus infection ( 5 ). Many viruses also induce mtROS production, which can aid viral replication and the release of progeny ( 6 ). The increase in ROS production is related to age-related diseases and a reduced lifespan ( 7 ).…”

Section: Introductionmentioning

confidence: 99%

A Review of the Potential Effects of Melatonin in Compromised Mitochondrial Redox Activities in Elderly Patients With COVID-19

et al. 2022

Front. Nutr.

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Melatonin, an endogenous indoleamine, is an antioxidant and anti-inflammatory molecule widely distributed in the body. It efficiently regulates pro-inflammatory and anti-inflammatory cytokines under various pathophysiological conditions. The melatonin rhythm, which is strongly associated with oxidative lesions and mitochondrial dysfunction, is also observed during the biological process of aging. Melatonin levels decline considerably with age and are related to numerous age-related illnesses. The signs of aging, including immune aging, increased basal inflammation, mitochondrial dysfunction, significant telomeric abrasion, and disrupted autophagy, contribute to the increased severity of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. These characteristics can worsen the pathophysiological response of the elderly to SARS-CoV-2 and pose an additional risk of accelerating biological aging even after recovery. This review explains that the death rate of coronavirus disease (COVID-19) increases with chronic diseases and age, and the decline in melatonin levels, which is closely related to the mitochondrial dysfunction in the patient, affects the virus-related death rate. Further, melatonin can enhance mitochondrial function and limit virus-related diseases. Hence, melatonin supplementation in older people may be beneficial for the treatment of COVID-19.

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Mitochondria-mediated oxidative stress during viral infection

Cited by 131 publications

References 111 publications

Hallmarks of Metabolic Reprogramming and Their Role in Viral Pathogenesis

Hallmarks of Metabolic Reprogramming and Their Role in Viral Pathogenesis

Aedes aegypti Aag-2 Cell Proteome Modulation in Response to Chikungunya Virus Infection

A Review of the Potential Effects of Melatonin in Compromised Mitochondrial Redox Activities in Elderly Patients With COVID-19

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