Porcine epidemic diarrhoea virus (PEDV) infection activates AMPK and JNK through TAK1 to induce autophagy and enhance virus replication

Wang, Jingxiang; Kan, Xianjin; Li, Xiaomei; Sun, Jing; Xu, Xiulong

doi:10.1080/21505594.2022.2127192

Cited by 6 publications

(2 citation statements)

References 69 publications

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“…Previous studies have demonstrated that viruses activate the JNK signaling pathway to up-regulate virus production and induce apoptosis. [35][36][37] Conversely, overexpressing JNK has been shown to inhibit viral replication and the virus-induced apoptosis. 38 In our study, we have identified that the JNK signaling pathway played a role in viral replication and delayed the virus-induced lethality.…”

Section: Discussionmentioning

confidence: 99%

Ben‐JNK signaling is required for host mortality during Periplaneta fuliginosa densovirus infection

Huang,

Qin,

Dong

et al. 2024

Pest Management Science

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BACKGROUNDCockroaches are widely acknowledged as significant vectors of pathogenic microorganisms. The densovirus PfDNV infects the smoky‐brown cockroach Periplaneta fuliginosa and causes host mortality, which identifies the PfDNV as a species‐specific and environmentally friendly biopesticide. However, although the biochemical characterization of PfDNV has been extensively studied, the immune response against PfDNV remains largely unclear.RESULTSHere, we investigated the replication of PfDNV and its associated pathological phenotype in the foregut and hindgut. Consequently, we dissected and performed transcriptome sequencing on the foregut, midgut, and hindgut separately. We revealed the up‐regulation of immune response signaling pathway JNK and apoptosis in response to viral infection. Furthermore, knockdown of the JNK upstream gene Ben resulted in a decrease in virus titer and delayed host mortality.CONCLUSIONTaken together, our findings provide evidence that the Ben‐JNK signaling plays a crucial role in PfDNV infection, leading to excessive apoptosis in intestinal tissues and ultimately resulting in the death of the host. Our results indicated that the host response to PfDNV fosters viral infection, thereby increasing host lethality. This underscores the potential of PfDNV as a viable, environmentally friendly biopesticide.This article is protected by copyright. All rights reserved.

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Section: Discussionmentioning

confidence: 99%

Ben‐JNK signaling is required for host mortality during Periplaneta fuliginosa densovirus infection

Huang,

Qin,

Dong

et al. 2024

Pest Management Science

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“…Viruses have the ability to manipulate some signal transduction pathways in host cells to promote their survival ( 38 ). Activation of AMPK played an important role in mediating PEDV-induced autophagy and supported viral replication ( 39 ). In this study, STRADA involved in the AMPK signaling pathway was significantly upregulated in the infected group, which has the function of aiding viral replication.…”

Section: Discussionmentioning

confidence: 99%

Transcriptomics yields valuable information regarding the response mechanisms of Chinese Min pigs infected with PEDV

Li,

Zhou,

Zhang

et al. 2023

Front. Vet. Sci.

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Porcine epidemic diarrhea virus (PEDV) causes porcine epidemic diarrhea (PED), a highly infectious disease, which has resulted in huge economic losses for the pig industry. To date, the pathogenic and immune response mechanism was not particularly clear. The purpose of this study was to investigate the pathogenic and immune responses of pigs infected with PEDV.In this study, 12 Min pigs were randomly selected without taking colostrum. At 3 days old, eight piglets were infected with 1 mL of PEDV solution (10 TCID50/ml), and the remaining four piglets were handled by 1 mL of 0.9% normal saline. Within the age of 7 days old, four piglets died and were considered as the death group. Correspondingly, four alive individuals were classified into the resistance group. Tissues of the duodenum, jejunum, ileum, colon, cecum, and rectum of piglets in the three groups were collected to measure the PEDV content. Additionally, the jejunum was used for the measurements and analyses of Hematoxylin-eosinstaining (HE), immunohistochemical sections, and transcriptomics. The phenotypes of Min piglets infected with PEDV showed that the viral copy numbers and jejunal damage had significant differences between the death and resistance groups. We also observed the transcriptome of the jejunum, and the differentially expressed (DE) analysis observed 6,585 DE protein-coding genes (PCGs), 3,188 DE long non-coding RNAs (lncRNAs), and 350 DE microRNAs (miRNAs), which were mainly involved in immune response and metabolic pathways. Furthermore, the specific expressed molecules for each group were identified, and 97 PCGs,108 lncRNAs, and 51 miRNAs were included in the ceRNA-regulated networks. By weighted gene co-expression network analysis (WGCNA) and transcription factor (TF) prediction, 27 significant modules and 32 significant motifs (E-value < 0.05) annotated with 519 TFs were detected. Of these TFs, 53 were DE PCGs. In summary, the promising key PCGs, lncRNAs, and miRNAs related to the pathogenic and immunological response of pigs infected with PEDV were detected and provided new insights into the pathogenesis of PEDV.

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Functions of MAP3Ks in antiviral immunity

et al. 2023

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Immune signal transduction is crucial to the body’s defense against viral infection. Recognition of pathogen-associated molecular patterns by pattern recognition receptors (PRRs) activates the transcription of interferon regulators and nuclear factor-κB (NF-κB); this promotes the release of interferons and inflammatory factors. Efficient regulation of type I interferon and NF-κB signaling by members of the mitogen-activated protein (MAP) kinase kinase kinase (MAP3K) family plays an important role in antiviral immunity. Elucidating the specific roles of MAP3K activation during viral infection is essential to develop effective antiviral therapies. In this review, we outline the specific regulatory mechanisms of MAP3Ks in antiviral immunity and discuss the feasibility of targeting MAP3Ks for the treatment of virus-induced diseases.

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Porcine epidemic diarrhoea virus (PEDV) infection activates AMPK and JNK through TAK1 to induce autophagy and enhance virus replication

Cited by 6 publications

References 69 publications

Ben‐JNK signaling is required for host mortality during Periplaneta fuliginosa densovirus infection

Ben‐JNK signaling is required for host mortality during Periplaneta fuliginosa densovirus infection

Transcriptomics yields valuable information regarding the response mechanisms of Chinese Min pigs infected with PEDV

Functions of MAP3Ks in antiviral immunity

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