Canine parvovirus induces G1/S cell cycle arrest that involves EGFR Tyr1086 phosphorylation

Dai, Xiaofeng; Zhang, Xuanhao; Miao, Yujie; Han, Ping; Zhang, Jianying

doi:10.1080/21505594.2020.1814091

Cited by 9 publications

(7 citation statements)

References 34 publications

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“…Viruses can control their infection and replication by regulating the G1/S and G2/M boundaries ( Miranda and Thompson, 2016 ; Qi et al, 2020 ). At present, CPV-related pathogenic molecular mechanisms are mainly focused on the effects of NS1 protein on apoptosis, cell cycle, and related signaling pathways ( Gupta et al, 2016 ; Lin et al, 2019 ; Dai et al, 2020 ). In addition, studies have shown that the cellular DNA damage response triggered by the invading single-stranded parvovirus can induce cell cycle arrest, thereby creating a favorable environment for viral replication ( Chen and Qiu, 2010 ; Lou et al, 2012 ; Xu et al, 2019 ; Zhang et al, 2019 ; Dai et al, 2020 ).…”

Section: Discussionmentioning

confidence: 99%

“…At present, CPV-related pathogenic molecular mechanisms are mainly focused on the effects of NS1 protein on apoptosis, cell cycle, and related signaling pathways ( Gupta et al, 2016 ; Lin et al, 2019 ; Dai et al, 2020 ). In addition, studies have shown that the cellular DNA damage response triggered by the invading single-stranded parvovirus can induce cell cycle arrest, thereby creating a favorable environment for viral replication ( Chen and Qiu, 2010 ; Lou et al, 2012 ; Xu et al, 2019 ; Zhang et al, 2019 ; Dai et al, 2020 ). While as an important component of the viral capsid, the CPV VP2 protein not only determines the host range of the virus ( Hueffer and Parrish, 2003 ), but also serves as a key protein in inducing the host immune defense mechanism ( Sarabandi and Pourtaghi, 2023 ).…”

Section: Discussionmentioning

confidence: 99%

“…Cell cycle arrest and apoptosis and related pathways play important roles in CPV replication. For example, CPV can trigger host G1/S cell cycle arrest via the EGFR (Y1086)/p27 and EGFR (Y1068)/STAT3/cyclin D1 axis ( Dai et al, 2020 ), and in the late stage of viral infection, nuclear assembly of the progeny capsids is accompanied by virus-induced cell cycle triggering host cell G2/M phase arrest ( Adeyemi et al, 2010 ; Ruiz et al, 2011 ; Mattola et al, 2022 ). Studies have shown that the eukaryotic chaperone T-complex protein-1 (TCP-1) ring complex (TRiC) plays an important role in the folding of many apoptosis and cell cycle-related proteins.…”

Section: Discussionmentioning

confidence: 99%

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Chaperonin TRiC/CCT subunit CCT7 is involved in the replication of canine parvovirus in F81 cells

Su,

Zhou,

et al. 2024

Front. Microbiol.

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Canine parvovirus (CPV) is one of the most common lethal viruses in canines. The virus disease is prevalent throughout the year, with high morbidity and mortality rate, causing serious harm to dogs and the dog industry. Previously, yeast two hybrid method was used to screen the protein chaperonin containing TCP-1 (CCT7) that interacts with VP2. However, the mechanism of interactions between CCT7 and VP2 on CPV replication remains unclear. In this study, we first verified the interaction between CCT7 and viral VP2 proteins using yeast one-to-one experiment and co-immunoprecipitation (CoIP) experiment. Laser confocal microscopy observation showed that CCT7 and VP2 were able to co-localize and were mostly localized in the cytoplasm. In addition, the study of VP2 truncated mutant found that the interaction region of VP2 with CCT7 was located between amino acids 231 and 320. Cycloheximide (CHX) chase experiments showed that CCT7 can improve the stability of VP2 protein. After further regulation of CCT7 expression in F81 cells, it was found that the expression level of VP2 protein was significantly reduced after knocking down CCT7 expression by RNA interference (RNAi) or HSF1A inhibitor, and increased after overexpressing host CCT7. The study reveals the role of VP2 interacting protein CCT7 in the replication process of CPV, which could provide a potential target for the prevention and control of CPV.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Chaperonin TRiC/CCT subunit CCT7 is involved in the replication of canine parvovirus in F81 cells

Su,

Zhou,

et al. 2024

Front. Microbiol.

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“…Inoculating cells with a 10-gradient sequentially diluted solutions of viral fluid at a step-size of 10 folds, and monitoring cells for 5 to 7 days until the occurrence of cytopathic effect (CPE) in 50% cells. TCID50 was calculated following previously recommended protocol 21 .…”

Section: Methodsmentioning

confidence: 99%

Cold Atmospheric Plasma Boosts Virus Multiplication via EGFR(Tyr1068) Phosphorylation-Mediated Control on Cell Mitophagy

Han¹,

Shen²,

Nan³

et al. 2022

Int. J. Biol. Sci.

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Objectives: Vaccination still remains as the most effective approach for preventing infectious diseases such as those caused by virus infection, with cell-based vaccine manufacturing being one flexible solution regarding the spectrum of infectious disorders it can prevent. Rapid cell-based virus propagation can enable high yield of vaccines against viral diseases that may offer critical values in the industry when handling emergent situations such as the ongoing viral disease pandemic. Methods: Through investigating the phenomenon and biological mechanism underlying redox-triggered cell survival towards enhanced viral particle production, this study explores novel strategies for improved yield of viral particles at a reduced cost to meet the increasing demand on cell-based vaccine manufacturing against viral diseases. Results: We found in this study that cold atmospheric plasma (CAP), composed of multiple reactive oxygen and nitrogen species including H 2 O 2 , could effectively enhance virus replication via triggering cell mitophagy that was dynamically modulated by the p-EGFR(Tyr1068)/p-Drp1(Ser616) axis using IBRV and MDBK as the virus and cell models, respectively; and removing H 2 O 2 can further enhance virus yield via releasing cells from excessive G 0 /G 1 cell cycle arrest. The observed efficacy of CAP was extended to other viruses such as CDV and CPV. Conclusion: This study provides experimental evidences supporting the use of CAP as a modulator of cell survival including mitophagy and mitochondria dynamics, and makes CAP an interesting and promising tool for enhancing the yield of viral vaccines if translated into the industry.

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“…CPV causes DNA disruption and interferes with the cell cycle, generating time to increase viral progenies leading to pathological consequences of infection, causing cell death after cell cycle arrest (Figure4) (49). In the Norden Laboratory Feline Kidney cell line (NLFK) and the Canine Fibroma cell line (A72), CPV causes cell cycle arrest in the S phase(49,58). Cell cycle arrest and DDR signaling evidently have significant role in canine parvovirus infections as inhibition of DDR interferes with viral replication and lowers the production of progeny(59).…”

mentioning

confidence: 99%

Canine Parvovirus and Its Non-Structural Gene 1 as Oncolytic Agents: Mechanism of Action and Induction of Anti-Tumor Immune Response

et al. 2021

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The exploration into the strategies for the prevention and treatment of cancer is far from complete. Apart from humans, cancer has gained considerable importance in animals because of increased awareness towards animal health and welfare. Current cancer treatment regimens are less specific towards tumor cells and end up harming normal healthy cells. Thus, a highly specific therapeutic strategy with minimal side effects is the need of the hour. Oncolytic viral gene therapy is one such specific approach to target cancer cells without affecting the normal cells of the body. Canine parvovirus (CPV) is an oncolytic virus that specifically targets and kills cancer cells by causing DNA damage, caspase activation, and mitochondrial damage. Non-structural gene 1 (NS1) of CPV, involved in viral DNA replication is a key mediator of cytotoxicity of CPV and can selectively cause tumor cell lysis. In this review, we discuss the oncolytic properties of Canine Parvovirus (CPV or CPV2), the structure of the NS1 protein, the mechanism of oncolytic action as well as role in inducing an antitumor immune response in different tumor models.

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Canine parvovirus induces G1/S cell cycle arrest that involves EGFR Tyr1086 phosphorylation

Cited by 9 publications

References 34 publications

Chaperonin TRiC/CCT subunit CCT7 is involved in the replication of canine parvovirus in F81 cells

Chaperonin TRiC/CCT subunit CCT7 is involved in the replication of canine parvovirus in F81 cells

Cold Atmospheric Plasma Boosts Virus Multiplication via EGFR(Tyr1068) Phosphorylation-Mediated Control on Cell Mitophagy

Canine Parvovirus and Its Non-Structural Gene 1 as Oncolytic Agents: Mechanism of Action and Induction of Anti-Tumor Immune Response

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