The Role of Epidermal Growth Factor Receptor Signaling Pathway during Bovine Herpesvirus 1 Productive Infection in Cell Culture

Qiu, Wen-Cai; Chang, Long; He, Yueqiu; Zhu, Liqian

doi:10.3390/v12090927

Cited by 9 publications

(11 citation statements)

References 51 publications

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“…Since EGFR does not affect JEV attachment and entry in hBMECs, how does EGFR facilitate JEV infection in hBMECs? It has been widely reported that EGFR participates in the regulation of host innate immunity during viral infection (Lupberger et al, 2013 ; Qiu et al, 2020 ; Wang et al, 2021 ). For example, respiratory virus (RSV) induced EGFR phosphorylation, which inhibited interferon regulatory factor 1 (IRF1)-regulate interferon-lambda (IFN-λ) production and breakdown of airway epithelium antiviral response (Kalinowski et al, 2018 ).…”

Section: Resultsmentioning

confidence: 99%

EGFR Activation Impairs Antiviral Activity of Interferon Signaling in Brain Microvascular Endothelial Cells During Japanese Encephalitis Virus Infection

et al. 2022

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The establishment of Japanese encephalitis virus (JEV) infection in brain microvascular endothelial cells (BMECs) is thought to be a critical step to induce viral encephalitis with compromised blood–brain barrier (BBB), and the mechanisms involved in this process are not completely understood. In this study, we found that epidermal growth factor receptor (EGFR) is related to JEV escape from interferon-related host innate immunity based on a STRING analysis of JEV-infected primary human brain microvascular endothelial cells (hBMECs) and mouse brain. At the early phase of the infection processes, JEV induced the phosphorylation of EGFR. In JEV-infected hBMECs, a rapid internalization of EGFR that co-localizes with the endosomal marker EEA1 occurred. Using specific inhibitors to block EGFR, reduced production of viral particles was observed. Similar results were also found in an EGFR-KO hBMEC cell line. Even though the process of viral infection in attachment and entry was not noticeably influenced, the induction of IFNs in EGFR-KO hBMECs was significantly increased, which may account for the decreased viral production. Further investigation demonstrated that EGFR downstream cascade ERK, but not STAT3, was involved in the antiviral effect of IFNs, and a lowered viral yield was observed by utilizing the specific inhibitor of ERK. Taken together, the results revealed that JEV induces EGFR activation, leading to a suppression of interferon signaling and promotion of viral replication, which could provide a potential target for future therapies for the JEV infection.

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Section: Resultsmentioning

confidence: 99%

EGFR Activation Impairs Antiviral Activity of Interferon Signaling in Brain Microvascular Endothelial Cells During Japanese Encephalitis Virus Infection

et al. 2022

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“…Two main signalling pathways enriched by the host gene set in the second positive module included G protein-coupled receptors and epidermal growth factor receptors (EGFR). These are involved in the pathogen pathophysiological processes (78, 79) and in mediating cellular entry of numerous pathogen cells (48), respectively. Generally, the functions related to this module have a role in immune pathogenesis by activities of innate and adaptive immune systems.…”

Section: Resultsmentioning

confidence: 99%

“…This process can stimulate the response of the innate immune system (47). GO enrichment analysis has shown that 380 genes across host clusters were enriched with functions which play essential roles in mediating cellular entry of pathogens ( e.g ., epidermal growth factor receptor (EGFR) signalling pathway (48), growth hormone receptor signalling pathway (49), mitochondrial ATP synthesis coupled electron transport (50), protein targeting to endoplasmic reticulum(51)), communication of bacteria with the host environment ( e.g ., positive regulation of establishment of protein localization(52)), control of infection ( e.g ., regulation of protein metabolic process(53)), invading pathogen ( e.g ., response to laminar fluid shear stress (54)), and co-opting host factors ( e.g ., viral gene expression (55)) that can be considered as potential targets in designing antibacterial therapies. Enriched functions were mostly observed at 24h and 4h pi in the host and pathogen, respectively, with mainly downregulated expression (Supplementary Table).…”

Section: Resultsmentioning

confidence: 99%

dSeqSb: A systems biology approach to decipher dynamics of host-pathogen interactions using temporal dual RNA-seq data

Dinarvand

Koch

Mouiee

et al. 2022

Preprint

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Infection triggers a dynamic cascade of reciprocal events between host and pathogen wherein the host activates complex mechanisms to recognise and kill pathogens while the pathogen adjusts its virulence and fitness to avoid eradication by the host. The interaction between the pathogen and the host results in large-scale changes in gene expression in both organisms. Dual RNA-seq, the simultaneous detection of host and pathogen transcripts, has become a leading approach to unravel complex molecular interactions between the host and the pathogen and is particularly informative for intracellular organisms. The amount of in vitro and in vivo dual RNA-seq data is rapidly growing which demands computational pipelines to effectively analyse such data. In particular, holistic, systems-level, and temporal analyses of dual RNA-seq data are essential to enable further insights into the host-pathogen transcriptional dynamics and potential interactions. Here, we developed an integrative network-driven bioinformatics pipeline, dRNASb, a systems biology-based computational pipeline to analyse temporal transcriptional clusters, incorporate molecular interaction networks (e.g., protein-protein interactions), identify topologically and functionally key transcripts in host and pathogen, and associate host and pathogen temporal transcriptome to decipher potential between-species interactions. The pipeline is applicable to various dual RNA-seq data from different species and experimental conditions. As a case study, we applied dRNASb to analyse temporal dual RNA-seq data of Salmonella-infected human cells, which enabled us to uncover genes contributing to the infection process and their potential functions and to identify potential host-pathogen interactions between host and pathogen genes. Overall, dRNASb has the potential to identify key genes involved in bacterial growth or host defence mechanisms for future uses as therapeutic targets.

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“…GO enrichment analysis has shown that 380 genes across host clusters were enriched with functions that play essential roles in mediating cellular entry of pathogens (e.g . epidermal growth factor receptor (EGFR) signalling pathway [ 46 ], growth hormone receptor signalling pathway [ 47 ], mitochondrial ATP synthesis coupled electron transport [ 48 ], protein targeting to the endoplasmic reticulum [ 49 ]), communication of bacteria with the host environment (e.g . positive regulation of establishment of protein localisation [ 50 ]), control of infection (e.g .…”

Section: Resultsmentioning

confidence: 99%

dRNASb: a systems biology approach to decipher dynamics of host-pathogen interactions using temporal dual RNA-seq data

et al. 2022

View full text Add to dashboard Cite

Infection triggers a dynamic cascade of reciprocal events between host and pathogen wherein the host activates complex mechanisms to recognise and kill pathogens while the pathogen often adjusts its virulence and fitness to avoid eradication by the host. The interaction between the pathogen and the host results in large-scale changes in gene expression in both organisms. Dual RNA-seq, the simultaneous detection of host and pathogen transcripts, has become a leading approach to unravelling complex molecular interactions between the host and the pathogen and is particularly informative for intracellular organisms. The amount of in vitro and in vivo dual RNA-seq data is rapidly growing, which demands computational pipelines to effectively analyse such data. In particular, holistic, systems-level, and temporal analyses of dual RNA-seq data are essential to enable further insights into the host-pathogen transcriptional dynamics and potential interactions. Here, we developed an integrative network-driven bioinformatics pipeline, dRNASb, a systems biology-based computational pipeline to analyse temporal transcriptional clusters, incorporate molecular interaction networks (e.g. protein-protein interactions), identify topologically and functionally key transcripts in host and pathogen, and associate host and pathogen temporal transcriptome to decipher potential between-species interactions. The pipeline is applicable to various dual RNA-seq data from different species and experimental conditions. As a case study, we applied dRNASb to analyse temporal dual RNA-seq data of Salmonella -infected human cells, which enabled us to uncover genes contributing to the infection process and their potential functions and to identify putative associations between host and pathogen genes during infection. Overall, dRNASb has the potential to identify key genes involved in bacterial growth or host defence mechanisms for future uses as therapeutic targets.

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The Role of Epidermal Growth Factor Receptor Signaling Pathway during Bovine Herpesvirus 1 Productive Infection in Cell Culture

Cited by 9 publications

References 51 publications

EGFR Activation Impairs Antiviral Activity of Interferon Signaling in Brain Microvascular Endothelial Cells During Japanese Encephalitis Virus Infection

EGFR Activation Impairs Antiviral Activity of Interferon Signaling in Brain Microvascular Endothelial Cells During Japanese Encephalitis Virus Infection

dSeqSb: A systems biology approach to decipher dynamics of host-pathogen interactions using temporal dual RNA-seq data

dRNASb: a systems biology approach to decipher dynamics of host-pathogen interactions using temporal dual RNA-seq data

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