Dengue virus induced autophagy is mediated by HMGB1 and promotes viral propagation

Chaudhary, Nidhi; Srivastava, Sachi; Gupta, Sunny; Menon, Manoj B.; Patel, Ashok Kumar

doi:10.1016/j.ijbiomac.2022.12.299

Cited by 10 publications

(6 citation statements)

References 46 publications

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“…ZIKV infection of human umbilical vein endothelial cells can modulate the AKT/mTOR and BECN1 signalling pathways to induce autophagy and enhance viral replication [40]. DENV was shown to induce autophagy by the BECN1/BCL2 pathway in A549 cells [41]. In this study, we examined the signalling pathways of autophagy induced by DTMUV, and the results indicated that DTMUV could induce autophagy in Neuro-2a cells via the ERK/mTOR and AMPK/mTOR signaling pathways.…”

Section: Discussionmentioning

confidence: 94%

Duck Tembusu virus induces incomplete autophagy via the ERK/mTOR and AMPK/mTOR signalling pathways to promote viral replication in neuronal cells

Wang

Jiang

Bao

et al. 2023

Preprint

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Duck Tembusu virus (DTMUV) is a neurotropic virus belonging to the genus Flavivirus, and causes massive economic losses to the poultry industry in China and neighbouring countries. Autophagy plays a pivotal role in cellular responses to pathogens and viral pathogenesis. However, little is known about the roles of autophagy in DTMUV replication and virus pathogenesis, especially in neuropathogenesis. In this study, mouse neuroblastoma cells (Neuro-2a) were used to establish a DTMUV infection cell model. Our experiments indicated that DTMUV infection induced incomplete autophagy in Neuro-2a cells. Then, autophagy induced by DTMUV was altered with different autophagy regulators, and we found that incomplete autophagy promoted DTMUV replication. Furthermore, we showed that DTMUV infection activated both the ERK and AMPK pathways, resulting in decreased phosphorylation levels of the autophagy repressor mTOR, subsequently leading to autophagic induction. In addition, we utilized ICR mice as the DTMUV-infected animal model to evaluate the autophagic responses in brain tissues and investigate the effects of autophagy on viral replication and tissue lesions. As a result, we confirmed that DTMUV induced incomplete autophagy in mouse brain tissues and that autophagy inducer treatment promoted DTMUV replication and aggravated DTMUV-induced lesions, whereas autophagy inhibitor treatment led to the opposite effects. Collectively, DTMUV infection induced incomplete autophagy through the ERK/mTOR and AMPK/mTOR signalling pathways to promote viral replication in mouse neuronal cells, and DTMUV-induced incomplete autophagy contributed to the neuropathogenesis of DTMUV.

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Section: Discussionmentioning

confidence: 94%

Duck Tembusu virus induces incomplete autophagy via the ERK/mTOR and AMPK/mTOR signalling pathways to promote viral replication in neuronal cells

Wang

Jiang

Bao

et al. 2023

Preprint

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“…Cytoplasmic HMGB1 interacts with Beclin 1 and ATG5 during inflammation by preventing calpain-mediated cleavage of these proteins, allowing autophagy to proceed ( Zhu et al., 2015 ). Dengue virus utilizes HMGB1/BECN1-dependent autophagy to enhance its propagation ( Chaudhary et al., 2023 ). HMGB1 in the nuclei is known to decompact the chromatin fibers to ensure easier access of the chromatin loci to the regulatory machineries ( Agresti and Bianchi, 2003 ).…”

Section: Discussionmentioning

confidence: 99%

Npro of classical swine fever virus enhances HMGB1 acetylation and its degradation by lysosomes to evade from HMGB1-mediated antiviral immunity

Han,

Xu,

Weng

et al. 2024

Virus Research

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“…For example, NDV infection triggers HMGB1 release to promote the inflammatory response, which largely contributes to pathogenic damage [ 53 ]. Dengue virus exploits HMGB1-mediated autophagy to enhance virus propagation [ 54 ]. JEV activates the MAPK pathway by restricting HMGB1 expression for viral replication [ 55 ].…”

Section: Discussionmentioning

confidence: 99%

HMGB1 is involved in viral replication and the inflammatory response in coxsackievirus A16-infected 16HBE cells via proteomic analysis and identification

Liu

Yang

et al. 2023

Virol J

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Coxsackievirus A16 (CV-A16) is still an important pathogen that causes hand, foot and mouth disease (HFMD) in young children and infants worldwide. Previous studies indicated that CV-A16 infection is usually mild or self-limiting, but it was also found that CV-A16 infection can trigger severe neurological complications and even death. However, there are currently no vaccines or antiviral compounds available to either prevent or treat CV-A16 infection. Therefore, investigation of the virus‒host interaction and identification of host proteins that play a crucial regulatory role in the pathogenesis of CV-A16 infection may provide a novel strategy to develop antiviral drugs. Here, to increase our understanding of the interaction of CV-A16 with the host cell, we analyzed changes in the proteome of 16HBE cells in response to CV-A16 using tandem mass tag (TMT) in combination with LC‒MS/MS. There were 6615 proteins quantified, and 172 proteins showed a significant alteration during CV-A16 infection. These differentially regulated proteins were involved in fundamental biological processes and signaling pathways, including metabolic processes, cytokine‒cytokine receptor interactions, B-cell receptor signaling pathways, and neuroactive ligand‒receptor interactions. Further bioinformatics analysis revealed the characteristics of the protein domains and subcellular localization of these differentially expressed proteins. Then, to validate the proteomics data, 3 randomly selected proteins exhibited consistent changes in protein expression with the TMT results using Western blotting and immunofluorescence methods. Finally, among these differentially regulated proteins, we primarily focused on HMGB1 based on its potential effects on viral replication and virus infection-induced inflammatory responses. It was demonstrated that overexpression of HMGB1 could decrease viral replication and upregulate the release of inflammatory cytokines, but deletion of HMGB1 increased viral replication and downregulated the release of inflammatory cytokines. In conclusion, the results from this study have helped further elucidate the potential molecular pathogenesis of CV-A16 based on numerous protein changes and the functions of HMGB1 Found to be involved in the processes of viral replication and inflammatory response, which may facilitate the development of new antiviral therapies as well as innovative diagnostic methods.

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Dengue virus induced autophagy is mediated by HMGB1 and promotes viral propagation

Cited by 10 publications

References 46 publications

Duck Tembusu virus induces incomplete autophagy via the ERK/mTOR and AMPK/mTOR signalling pathways to promote viral replication in neuronal cells

Duck Tembusu virus induces incomplete autophagy via the ERK/mTOR and AMPK/mTOR signalling pathways to promote viral replication in neuronal cells

Npro of classical swine fever virus enhances HMGB1 acetylation and its degradation by lysosomes to evade from HMGB1-mediated antiviral immunity

HMGB1 is involved in viral replication and the inflammatory response in coxsackievirus A16-infected 16HBE cells via proteomic analysis and identification

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