Mitophagy in Viral Infections

Mao, Xia; Ma, Gang; Li, Min; Wei, Jiwu

doi:10.1089/dna.2014.2567

Cited by 9 publications

(12 citation statements)

References 53 publications

(56 reference statements)

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“…Here, we demonstrated complete mitophagy by colocalization analysis of mitophagosomes with lysosomes and a dual fluorescence reporter (Mito-mRFP-EGFP) in CSFV-infected cells. This finding is consistent with several recent reports demonstrating complete mitophagy in virus-infected cells [31]. …”

Section: Discussionsupporting

confidence: 94%

“…In contrast to non-selectively autophagic degradation of proteins and organelles for supplying cellular energy, selective autophagy consists of the recruitment of specific adaptor proteins to targets and their delivery by autophagosomes for degradation [64]. Our data offer new evidence for selective autophagy of mitochondria triggered by viral infection [31]. …”

Section: Discussionmentioning

confidence: 93%

“…A number of viral proteins target to mitochondria and interact with mitochondrial proteins, resulting in ROS accumulation, mitochondrial Ca 2+ overload, the collapse of mitochondrial transmembrane potential, and subsequent mitochondrial dysfunction [21–25]. Notably, several viruses such as hepatitis C virus, hepatitis B virus and influenza A virus can trigger virus-specific mitophagy to balance aberrant mitochondrial dynamics [26–31]. …”

Section: Introductionmentioning

confidence: 99%

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CSFV induced mitochondrial fission and mitophagy to inhibit apoptosis

Gou

Zhao

et al. 2017

Oncotarget

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Classical swine fever virus (CSFV), which causes typical clinical characteristics in piglets, including hemorrhagic syndrome and immunosuppression, is linked to hepatitis C and dengue virus. Oxidative stress and a reduced mitochondrial transmembrane potential are disturbed in CSFV-infected cells. The balance of mitochondrial dynamics is essential for cellular homeostasis. In this study, we offer the first evidence that CSFV induces mitochondrial fission and mitophagy to inhibit host cell apoptosis for persistent infection. The formation of mitophagosomes and decline in mitochondrial mass relevant to mitophagy were detected in CSFV-infected cells. CSFV infection increased the expression and mitochondrial translocation of Pink and Parkin. Upon activation of the PINK1 and Parkin pathways, Mitofusin 2 (MFN2), a mitochondrial fusion mediator, was ubiquitinated and degraded in CSFV-infected cells. Mitophagosomes and mitophagolysosomes induced by CSFV were, respectively, observed by the colocalization of LC3-associated mitochondria with Parkin or lysosomes. In addition, a sensitive dual fluorescence reporter (mito-mRFP-EGFP) was utilized to analyze the delivery of mitophagosomes to lysosomes. Mitochondrial fission caused by CSFV infection was further determined by mitochondrial fragmentation and Drp1 translocation into mitochondria using a confocal microscope. The preservation of mitochondrial proteins, upregulated apoptotic signals and decline of viral replication resulting from the silencing of Drp1 and Parkin in CSFV-infected cells suggested that CSFV induced mitochondrial fission and mitophagy to enhance cell survival and viral persistence. Our data for mitochondrial fission and selective mitophagy in CSFV-infected cells reveal a unique view of the pathogenesis of CSFV infection and provide new avenues for the development of antiviral strategies.

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Section: Discussionsupporting

confidence: 94%

Section: Discussionmentioning

confidence: 93%

Section: Introductionmentioning

confidence: 99%

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CSFV induced mitochondrial fission and mitophagy to inhibit apoptosis

Gou

Zhao

et al. 2017

Oncotarget

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“…Apoptosis is suppressed by mitophagy by a wide variety of viruses during infection [ 16 , 29 – 33 ]. To determine whether mitophagy attenuates apoptosis during TGEV infection, IPEC-J2 cells were simultaneously stained with Propidium Iodide (PI) and Annexin V at 0 h, 24 h, and 48 h post-infection, and analyzed by flow cytometry.…”

Section: Resultsmentioning

confidence: 99%

Mitophagy in TGEV infection counteracts oxidative stress and apoptosis

et al. 2016

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The intestinal epithelial cells contain a large number of mitochondria for persisting absorption and barrier function. Selective autophagy of mitochondria (mitophagy) plays an important role in the quality control of mitochondria and maintenance of cell homeostasis. Transmissible gastroenteritis virus (TGEV) is a porcine enteropathogenic coronavirus which induces malabsorption and lethal watery diarrhea in suckling piglets. The role of mitophagy in the pathological changes caused by TGEV infection is unclear. Here, we report that TGEV induces mitophagy to suppress oxidative stress and apoptosis induced by viral infection in porcine epithelial cells (IPEC-J2). We observe that TGEV infection induce mitochondrial injury, abnormal morphology, complete mitophagy, and without obvious apoptosis after TGEV infection. Meanwhile, TGEV also induces DJ-1 and some antioxidant genes upregulation to suppress oxidative stress induced by viral infection. Furthermore, silencing DJ-1 inhibit mitophagy and increase apoptosis after TGEV infection. In addition, we demonstrate for the first time that viral nucleocapsid protein (N) is located in mitochondria and mitophagosome during virus infection or be expressed alone. Those results provide a novel perspective for further improvement of prevention and treatment in TGEV infection. These results suggest that TGEV infection induce mitophagy to promote cell survival and possibly viral infection.

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“…Upregulation of mitophagy and degradation of the mitochondrial antiviral signalling protein (MAVS) in order to attenuate the antiviral immune response in non-small cell lung cancer (NSCLC) cells was reported upon measles virus infection [83]. The expression of matrix protein (M) of human parainfluenza virus type 3 (HPIV3) in HEK293T and HeLa cells was reported to induce mitophagy resulting in the suppression of type1 interferon response [84].…”

Section: Effect On Mitochondrial Morphology and Intracellular Distribmentioning

confidence: 99%

Organelle dynamics and viral infections: at cross roads

Glingston

Deb

Kumar

et al. 2019

Microbes and Infection

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Viruses are obligate intracellular parasites of the host cells. A commonly accepted view is the requirement of internal membranous structures for various aspects of viral life cycle. Organelles enable favourable intracellular environment for several viruses. However, studies reporting organelle dynamics upon viral infections are scant. In this review, we aim to summarize and highlight modulations caused to various organelles upon viral infection or expression of its proteins.

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Mitophagy in Viral Infections

Cited by 9 publications

References 53 publications

CSFV induced mitochondrial fission and mitophagy to inhibit apoptosis

CSFV induced mitochondrial fission and mitophagy to inhibit apoptosis

Mitophagy in TGEV infection counteracts oxidative stress and apoptosis

Organelle dynamics and viral infections: at cross roads

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