Modulation of Mitochondria During Viral Infections

Reshi, Latif; Wang, Hao Ven; Hong, Jiann Ruey

doi:10.5772/intechopen.73036

Cited by 11 publications

(13 citation statements)

References 88 publications

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“…Of note, the STING induction of type I IFN responses is a process that occurs only when the cell are not mobilizing apoptotic caspases (85). Thus, it evidences the importance of the cGAS-STING-IRF3 axis during neuropathology, as traumatic brain injury and hypoxia (145)(146)(147).…”

Section: A Sting In the Brainmentioning

confidence: 85%

Unraveling the Link Between Mitochondrial Dynamics and Neuroinflammation

et al. 2021

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Neuroinflammatory and neurodegenerative diseases are a major public health problem worldwide, especially with the increase of life-expectancy observed during the last decades. For many of these diseases, we still lack a full understanding of their etiology and pathophysiology. Nonetheless their association with mitochondrial dysfunction highlights this organelle as an important player during CNS homeostasis and disease. Markers of Parkinson (PD) and Alzheimer (AD) diseases are able to induce innate immune pathways induced by alterations in mitochondrial Ca2+ homeostasis leading to neuroinflammation. Additionally, exacerbated type I IFN responses triggered by mitochondrial DNA (mtDNA), failures in mitophagy, ER-mitochondria communication and mtROS production promote neurodegeneration. On the other hand, regulation of mitochondrial dynamics is essential for CNS health maintenance and leading to the induction of IL-10 and reduction of TNF-α secretion, increased cell viability and diminished cell injury in addition to reduced oxidative stress. Thus, although previously solely seen as power suppliers to organelles and molecular processes, it is now well established that mitochondria have many other important roles, including during immune responses. Here, we discuss the importance of these mitochondrial dynamics during neuroinflammation, and how they correlate either with the amelioration or worsening of CNS disease.

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Section: A Sting In the Brainmentioning

confidence: 85%

Unraveling the Link Between Mitochondrial Dynamics and Neuroinflammation

et al. 2021

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“…Initially, viral components (capsid, nucleic acids) are detected by intracellular receptors (PRRs) that activate proinflammatory responses ( Sparrer and Gack, 2015 ; Lee et al, 2019 ; Matz et al, 2019 ). Mitochondria regulate viral detection and subsequent immune responses through the activation of the MAVS protein ( Vazquez et al, 2015 ), the release of mtDNA ( Wu et al, 2019 ; Riley and Tait, 2020 ), or through MAM modulation ( Reshi et al, 2018 ). MAVS activation is a key event following infection with RNA viruses.…”

Section: Mitochondria-dependent Strategies Of Immune Regulation By Homentioning

confidence: 99%

Mitochondria Targeted Viral Replication and Survival Strategies—Prospective on SARS-CoV-2

et al. 2020

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SARS-CoV-2 is a positive sense RNA coronavirus that constitutes a new threat for the global community and economy. While vaccines against SARS-CoV-2 are being developed, the mechanisms through which this virus takes control of an infected cell to replicate remains poorly understood. Upon infection, viruses completely rely on host cell molecular machinery to survive and replicate. To escape from the immune response and proliferate, viruses strategically modulate cellular metabolism and alter subcellular organelle architecture and functions. One way they do this is by modulating the structure and function of mitochondria, a critical cellular metabolic hub but also a key platform for the regulation of cellular immunity. This versatile nature of mitochondria defends host cells from viruses through several mechanisms including cellular apoptosis, ROS signaling, MAVS activation and mitochondrial DNA-dependent immune activation. These events are regulated by mitochondrial dynamics, a process by which mitochondria alter their structure (including their length and connectivity) in response to stress or other cues. It is therefore not surprising that viruses, including coronaviruses hijack these processes for their survival. In this review, we highlight how positive sense RNA viruses modulate mitochondrial dynamics and metabolism to evade mitochondrial mediated immune response in order to proliferate.

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“…The ER‐mimicking strategy of HepC allows the virus not only to hide from defence mechanisms but also to travel through the cytoplasm with a VAP key that can provide access to membranes of other organelles (mimicking an ER ‘second‐order’), exploiting them as a seemingly welcomed guest. For example, viruses are known to hijack mitochondria, the powerhouse of the cell, and take advantage of their functions (suggested reviews, Anand and Tikoo, 2013; Khan et al ., 2015; Reshi et al ., 2018; Tiku et al ., 2020).…”

Section: Possibility Of Host Fungal Er Contacts With Bacterial Endosymbiontsmentioning

confidence: 99%

A potential third‐order role of the host endoplasmic reticulum as a contact site in interkingdom microbial endosymbiosis and viral infection

Almeida¹

2021

Environ Microbiol Rep

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Summary The normal functioning of eukaryotic cells depends on the compartmentalization of metabolic processes within specific organelles. Interactions among organelles, such as those between the endoplasmic reticulum (ER) – considered the largest single structure in eukaryotic cells – and other organelles at membrane contact sites (MCSs) have also been suggested to trigger synergisms, including intracellular immune responses against pathogens. In addition to the ER‐endogenous functions and ER‐organelle MCSs, we present the perspective of a third‐order role of the ER as a host contact site for endosymbiotic microbial non‐pathogens and pathogens, from endosymbiont bacteria to parasitic protists and viruses. Although understudied, ER‐endosymbiont interactions have been observed in a range of eukaryotic hosts, including protists, plants, algae, and metazoans. Host ER interactions with endosymbionts could be an ER function built from ancient, conserved mechanisms selected for communicating with mutualistic endosymbionts in specific life cycle stages, and they may be exploited by pathogens and parasites. The host ER‐‘guest’ interactome and traits in endosymbiotic biology are briefly discussed. The acknowledgment and understanding of these possible mechanisms might reveal novel evolutionary perspectives, uncover the causes of unexplained cellular disorders and suggest new pharmacological targets.

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Modulation of Mitochondria During Viral Infections

Cited by 11 publications

References 88 publications

Unraveling the Link Between Mitochondrial Dynamics and Neuroinflammation

Unraveling the Link Between Mitochondrial Dynamics and Neuroinflammation

Mitochondria Targeted Viral Replication and Survival Strategies—Prospective on SARS-CoV-2

A potential third‐order role of the host endoplasmic reticulum as a contact site in interkingdom microbial endosymbiosis and viral infection

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