Induction of Apoptosis in Murine Coronavirus-Infected Cultured Cells and Demonstration of E Protein as an Apoptosis Inducer

An, Sungwhan; Chen, Chun‐Jen; Yu, Xuekui; Leibowitz, Julian L.; Makino, Shinji

doi:10.1128/jvi.73.9.7853-7859.1999

Cited by 109 publications

(83 citation statements)

References 64 publications

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“…Prolonged ER stress is known to activate related signaling to trigger ER stress-dependent apoptotic cell death (Tabas and Ron, 2011). It has also been demonstrated that Coronavirus proteins induce apoptosis in vitro and in vivo (An et al, 1999;DeDiego et al, 2011). Our results so far suggest that ORF3 might induce the apoptosis via triggering the ER stress.…”

Section: Pedv Orf3 Protein Has No Effect On Apoptosissupporting

confidence: 57%

Porcine epidemic diarrhea virus ORF3 protein causes endoplasmic reticulum stress to facilitate autophagy

Zou

Duan

et al. 2019

Veterinary Microbiology

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A B S T R A C TPorcine epidemic diarrhea virus (PEDV), the causative agent of PED, is an enveloped, positive-stranded RNA virus in the genus Alphacoronavirus, family Coronaviridae, order Nidovirales. PEDV non-structural accessory protein ORF3 is an ion channel related to viral infectivity and pathogenicity. Our previous study showed that PEDV ORF3 has expression characteristic of aggregation in cytoplasm, but its biological function remains elusive. Thus in this study, we initiated the construction of various vectors to express ORF3, and found ORF3 localized in the cytoplasm in the aggregation manner. Subsequently, confocal microscopy analysis showed that the aggregated ORF3 localized in endoplasmic reticulum (ER) to trigger ER stress response via up-regulation of GRP78 protein expression and activation of PERK-eIF2α signaling pathway. In addition, our results showed that PEDV ORF3 could induce the autophagy through inducing conversion of LC3-I to LC3-II, but couldn't influence the apoptosis. In contrast, conversion of LC3-I/LC3-II could be significantly inhibited by 4-PBA, an ER stress inhibitor, indicating that ORF3-induced autophagy is dependent on ER stress response. This work not only provides some new findings for the biological function of the PEDV ORF3 protein, but also help us for the further understanding the molecular interaction between PEDV ORF3 protein and cells.

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Section: Pedv Orf3 Protein Has No Effect On Apoptosissupporting

confidence: 57%

Porcine epidemic diarrhea virus ORF3 protein causes endoplasmic reticulum stress to facilitate autophagy

Zou

Duan

et al. 2019

Veterinary Microbiology

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“…Both processes have been previously described in FIPV-infected cats (Haagmans et al, 1996). Recent studies have shown apoptosis is a common feature in the pathogenesis of infection for several Coronaviridae members (An et al, 1999;Belyavsky et al, 1998;Liu et al, 2001;Sirinarumitr et al, 1998). FIPV, in particular, induces lymphocyte apoptosis predominantly in the CD3+ T-cell population (Haagmans et al, 1996).…”

Section: Tissue Distribution Of Fipv Rna and Histologic Lesionsmentioning

confidence: 75%

In vivo cytokine response to experimental feline infectious peritonitis virus infection

Dean

Olivry

Stanton

et al. 2003

Veterinary Microbiology

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Feline infectious peritonitis virus (FIPV) is a coronavirus that causes sporadic fatal disease in cats characterized by vasculitis, granulomatous inflammation and effusive pleuritis/peritonitis. Histologic changes in lymphoid tissues include lymphoid hyperplasia, lymphoid depletion, histiocytosis, and granuloma formation. Although viremia occurs, histologic lesions are not found uniformly throughout lymphoid tissues. We used experimental infection of cats with a highly pathogenic FIPV isolate, UCD8, to study histologic lesions, virus replication, and cytokine expression in multiple lymphoid tissues during the effusive phase of disease. Viral RNA was found in 76% of central tissues (mediastinal lymph node, spleen, mesenteric lymph node) examined, as compared to 27% of peripheral tissues (popliteal lymph node, cervical lymph node, femoral bone marrow). All tissues positive for virus replication also demonstrated lymphoid depletion. Generally, affected tissues had lower levels of IL-4 and IL-12-p40 mRNA and higher levels of IL-10 mRNA. Although no differences in IFN-gamma or TNF-alpha mRNA were measured, TNF-alpha protein expression was greater in affected tissues and demonstrated a shift in the source of TNF-alpha from macrophages to lymphocytes. Together, these results colocalize FIPV replication, lymphocyte depletion in tissues, and alterations in cytokine transcription and translation. A possible role for TNF-alpha in the previously described FIPV-induced lymphocyte apoptosis is also suggested.

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“…Several studies have claimed the involvement of viroporins in virus induced programmed cell death such as the case with coronavirus E protein and picornavirus 2B viroporin [54].…”

Section: Viroporins and Their Role In The Virus Life Cyclementioning

confidence: 99%

Viroporins and inflammasomes: A key to understand virus-induced inflammation

Farag

Breitinger

Azizi

2020

The International Journal of Biochemistry & Cell Biology

100

110

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J o u r n a l P r e -p r o o f Highlights  The article provides a summary on cellular receptors involved in virus immunity.  It presents an overview of the current understanding of inflammasomes complex activation, comparing its different types with special focus on NLRP3.  The article summarizes key findings on viroporins, a novel class of viral proteins and their role in the virus life cycle and host cell interactions.  The article sheds the light on the correlation between viroporins and inflammasomes activation and their possible contribution to aggravated inflammatory cytokines production.  The article proposes targeting inflammasomes in combination with viroporin inhibitors in virus-induced disease as an emerging attractive therapeutic option. Abstract Viroporins are virus encoded proteins that alter membrane permeability and can trigger subsequent cellular signals. Oligomerization of viroporin subunits results in formation of a hydrophilic pore which facilitates ion transport across host cell membranes. These viral channel proteins may be involved in different stages of the virus infection cycle. J o u r n a l P r e -p r o o f List of abbreviationsAIM Absent in melanoma ASC Apoptosis-associated speck-like protein containing a carboxy-terminal CARD ATP Adenosine triphosphate BMDC Bone marrow derived dendritic cells BMM Bone marrow derived macrophages CARD Caspase activation and recruitment domain CD Cluster of differentiation CoV Coronavirus CSFV Classical swine fever virus DAMPs Danger associated molecular patterns DC Dendritic cells EMCV Encephalomyocarditis virus HCV Hepatitis C virus HIV Human immune deficiency virus LPS Lipopolysaccharide LRR Leucine rich repeats MAL MyD88-adaptor-like MAM Mitochondrial-associated membrane MAVS Mitochondrial antiviral signaling protein MDA5 Melanoma differentiation-associated protein 5 MERS Middle East respiratory syndrome-related coronavirus MHC Major histocompatibility complex J o u r n a l P r e -p r o o f MSU Monosodium urate MyD88 Myeloid differentiation primary response 88 NADPH Nicotinamide adenine dinucleotide phosphate NALP NACHT, LRR and PYD domains-containing protein NFκB Nuclear factor kappa b NLR Nucleotide-binding domain, leucine-rich repeat NLRP3 NLR family, pyrin domain containing 3 Nod Nucleotide oligomerization domain PAMP Pathogen associated molecular patterns PRR Pattern recognition receptors PYD Pyrin domain RIG-1 Retinoic acid-inducible gene I RLR RIG-1 like receptor ROS Reactive Oxygen species RSV Respiratory syncytial virus

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Induction of Apoptosis in Murine Coronavirus-Infected Cultured Cells and Demonstration of E Protein as an Apoptosis Inducer

Cited by 109 publications

References 64 publications

Porcine epidemic diarrhea virus ORF3 protein causes endoplasmic reticulum stress to facilitate autophagy

Porcine epidemic diarrhea virus ORF3 protein causes endoplasmic reticulum stress to facilitate autophagy

In vivo cytokine response to experimental feline infectious peritonitis virus infection

Viroporins and inflammasomes: A key to understand virus-induced inflammation

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