Mitochondria as a Favourite Organelle for Invading Viruses

Reshi, Latif; Hong, Jiann Ruey

doi:10.4172/2168-9547.1000181

Cited by 12 publications

(25 citation statements)

References 117 publications

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“…For example, the mitochondrial anti-viral signaling (MAVS) protein can regulate the powerful NF-κB and interferon pathways after interacting with the viral RNA-sensing protein retinoic acid-inducible gene I (RIG-I), which are activated by virus-derived dsRNA [23]. Because of the key importance of mitochondria in apoptosis, cell metabolism and immune response, they are also a highly attractive target for many viral pathogens to manipulate in various manners to increase overall pathogen survival and thus pathogenesis [24].…”

Section: Introductionmentioning

confidence: 99%

The Cellular Localization of the p42 and p46 Oligoadenylate Synthetase 1 Isoforms and Their Impact on Mitochondrial Respiration

Skrivergaard

Jensen

Rolander

et al. 2019

Viruses

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The importance of the IFN-induced oligoadenylate synthetase (OAS) proteins and the OAS/RNase L pathway in the innate response against viral pathogens is well-established, however the observed differences in anti-viral activity between the human OAS1 p46 and p42 isoforms are not fully understood. The protein expression of these isoforms is determined by the SNP rs10774671, either being an A or a G allele resulting in expression of either the p42 or the p46 isoform. Using fluorescence microscopy and immunoblot analysis of fractionated cell samples, we show here that the CaaX motif is of key importance to the cellular localization. The OAS1 p42 isoform is mainly located in the cytosol, whereas the p46 isoform with a C-terminal CaaX motif is translocated to membranous organelles, like the mitochondria. We furthermore observed differences between p42 and p46 in their effect on mitochondrial physiology using high resolution respirometry and fluorometry. Overexpression of OAS1 p42 and IFN-β treatment of HeLa cells (AA genotype) resulted in significantly increased respiration, which was not seen with p46 overexpression. The difference in subcellular localization and mitochondrial effect of these two OAS1 isoforms might help to explain the anti-viral mechanisms that differentiate these proteins.

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Section: Introductionmentioning

confidence: 99%

The Cellular Localization of the p42 and p46 Oligoadenylate Synthetase 1 Isoforms and Their Impact on Mitochondrial Respiration

Skrivergaard

Jensen

Rolander

et al. 2019

Viruses

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“…On the other hand, IAP can inhibit the caspase-3 activation [88] but it is suppressed by the Smac/ DIABLO molecule, which is released from mitochondria [24]. Finally, if viruses entering or expressing, they can also trigger proapoptotic signaling (indicated by black lines) or block anti-apoptotic signaling (indicated by red lines) via whole virus or viral gene productions in mammalian viruses, which is associated with activation of caspase-dependent [9] and caspase-independent executioner mechanisms [2], leads to cell death by viral genes from RNA and DNA viruses, respectively for inducing some damaged or human diseases [4,27].…”

Section: Role Of Ros In Viral Diseasesmentioning

confidence: 99%

“…The numerous functions of mitochondria make them indispensable to the cell, so when a virus "hijacks" mitochondrial function, it allows it to control the whole cell. Mitochondria have important roles in several signal transduction pathways [18,19], the process of aging [20], regulation of different biochemical pathways related to cell metabolism [21,22], PCD [23,24], development [25,26], the pathogenesis of numerous diseases immune responses [19], and cell cycle control [19,27]. The circular mitochondrial genome encodes 13 polypeptides, 2 rRNAs, and 22 tRNAs.…”

Section: Mitochondrial Functionsmentioning

confidence: 99%

“…The circular mitochondrial genome encodes 13 polypeptides, 2 rRNAs, and 22 tRNAs. All of these mtDNA products are essential for function of the ETC and the generation of ATP by oxidative phosphorylation [9,27], although many proteins from the nuclear genome are also required. Thus, any injury to mtDNA can affect the whole cell.…”

Section: Mitochondrial Functionsmentioning

confidence: 99%

“…Thus, several recent models based on in vivo and in vitro studies explain the mechanisms underlying the maintenance and loss of the MMP. A loss of the MMP by any mechanism leads to functional and structural collapse of the mitochondria and cell death [27]. A recent study for first time has shown that dengue virus (DV) infection of human hepatoma cell line (HepG2) leads alteration in the bioenergetic function of mitochondrial morphology leading to MMP loss [28].…”

Section: Loss Of Mitochondrial Membrane Potentialmentioning

confidence: 99%

See 2 more Smart Citations

Modulation of Mitochondria During Viral Infections

Reshi¹,

Wang²,

Hong³

2018

Mitochondrial Diseases

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Mitochondria are organelles critical for cell survival because they produce ATP and modulate programmed cell death (PCD) pathways. PCD pathways are important in many clinical disorders, such as ischemia/reperfusion injuries, trauma, and toxic/metabolic syndromes, as well as in chronic neurodegenerative conditions, such as amyotrophic lateral sclerosis, Alzheimer's disease, Parkinson's disease, and Huntington's disease. Moreover, many viruses and other pathogens target the mitochondria. Viruses induce the production of various proteins in their hosts that have proapoptotic and anti-apoptotic activities, depending on the cellular environment. More specifically, many viruses that target mitochondria regulate the balance between the anti-and proapoptotic Bcl-2 family proteins and thereby increase their own survival within the host cell. Recent studies indicated that mitochondria centralize several critical innate immune responses based on the presence of several important signaling proteins within the mitochondria: mitochondrial antiviral signaling (MAVS), stimulation of interferon genes (STING), and NLR family member X1. Therefore, mitochondria are not only vital because they regulate cell survival and death but also they have broad roles in the control of cell functions following pathogen invasion. This chapter highlights the tight interplay between viral infection and mitochondria.

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Aedes aegypti microRNA, miR-2944b-5p interacts with 3'UTR of chikungunya virus and cellular target vps-13 to regulate viral replication

2019

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Background RNA interference is among the most important mechanisms that serve to restrict virus replication within mosquitoes, where microRNAs (miRNAs) are important in regulating viral replication and cellular functions. These miRNAs function by binding to complementary sequences mostly in the untranslated regions of the target. Chikungunya virus (CHIKV) genome consists of two open reading frames flanked by 5′ and 3′ untranslated regions on the two sides. A recent study from our laboratory has shown that Aedes miRNAs are regulated during CHIKV infection. The present study was undertaken to further understand the role of these miRNAs in CHIKV replication. Methods/Findings We observe that miR-2944b-5p binds to the 3′ untranslated region of CHIKV and the binding is abated when the binding sites are abolished. Loss-of-function studies of miR-2944b-5p using antagomirs, both in vitro and in vivo , reveal an increase in CHIKV viral replication, thereby directly implying a role of miR-2944b-5p in CHIKV replication. We further showed that the mitochondrial membrane potential of the mosquito cells is maintained by this miRNA during CHIKV replication, and cellular factor vps-13 plays a contributing role. Conclusions Our study has opened new avenues to understand vector-virus interactions and provides novel insights into CHIKV replication in Aedes aegypti . Furthermore, our study has shown miR-2944b-5p to be playing role, where one of its target vps-13 also contributes, in maintaining mitochondrial membrane potential in Aedes aegypti .

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Mitochondria as a Favourite Organelle for Invading Viruses

Cited by 12 publications

References 117 publications

The Cellular Localization of the p42 and p46 Oligoadenylate Synthetase 1 Isoforms and Their Impact on Mitochondrial Respiration

The Cellular Localization of the p42 and p46 Oligoadenylate Synthetase 1 Isoforms and Their Impact on Mitochondrial Respiration

Modulation of Mitochondria During Viral Infections

Aedes aegypti microRNA, miR-2944b-5p interacts with 3'UTR of chikungunya virus and cellular target vps-13 to regulate viral replication

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