Correction: EBV induces persistent NF-κB activation and contributes to survival of EBV-positive neoplastic T- or NK-cells

Takada, Honami; Imadome, Ken‐Ichi; Shibayama, Haruna; Yoshimori, Mayumi; Wang, Ludan; Saitoh, Yasunori; Uota, Shin; Shoji, Yasuhiro; Koyama, Takatoshi; Shimizu, Norio; Yamamoto, Kouhei; Fujiwara, Shigeyoshi; Miura, Osamu; Arai, Ayako

doi:10.1371/journal.pone.0182682

Cited by 11 publications

(6 citation statements)

References 1 publication

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“…Our finding that PRV triggers persistent NF-B activation in infected cells-in porcine, bovine, and rabbit epithelial cell lines as well as in primary porcine respiratory epithelial cells-indicates that this may be a common feature of several herpesviruses. Indeed, persistent NF-B activation has been reported for HSV-1 (28,63), another alphaherpesvirus, and for members of other herpesvirus subfamilies, including the betaherpesvirus HCMV (64) and the gammaherpesvirus EBV (65). Despite the apparent conservation of persistent NF-B activation among different herpesviruses, the function of NF-B in virus replication is still incompletely understood.…”

Section: Discussionmentioning

confidence: 99%

Pseudorabies Virus Infection of Epithelial Cells Leads to Persistent but Aberrant Activation of the NF-κB Pathway, Inhibiting Hallmark NF-κB-Induced Proinflammatory Gene Expression

Romero

Waesberghe

Favoreel

2020

J Virol

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The nuclear factor kappa B (NF-κB) is a potent transcription factor, activation of which typically results in robust proinflammatory signaling and triggering of fast negative feedback modulators to avoid excessive inflammatory responses. Here, we report that infection of epithelial cells, including primary porcine respiratory epithelial cells, with the porcine alphaherpesvirus pseudorabies virus (PRV) results in the gradual and persistent activation of NF-κB, illustrated by proteasome-dependent degradation of the inhibitory NF-κB regulator IκB and nuclear translocation and phosphorylation of the NF-κB subunit p65. PRV-induced persistent activation of NF-κB does not result in expression of negative feedback loop genes, like the gene for IκBα or A20, and does not trigger expression of prototypical proinflammatory genes, like the gene for tumor necrosis factor alpha (TNF-α) or interleukin-6 (IL-6). In addition, PRV infection inhibits TNF-α-induced canonical NF-κB activation. Hence, PRV infection triggers persistent NF-κB activation in an unorthodox way and dramatically modulates the NF-κB signaling axis, preventing typical proinflammatory gene expression and the responsiveness of cells to canonical NF-κB signaling, which may aid the virus in modulating early proinflammatory responses in the infected host. IMPORTANCE The NF-κB transcription factor is activated via different key inflammatory pathways and typically results in the fast expression of several proinflammatory genes as well as negative feedback loop genes to prevent excessive inflammation. In the current report, we describe that infection of cells with the porcine alphaherpesvirus pseudorabies virus (PRV) triggers a gradual and persistent aberrant activation of NF-κB, which does not result in expression of hallmark proinflammatory or negative feedback loop genes. In addition, although PRV-induced NF-κB activation shares some mechanistic features with canonical NF-κB activation, it also shows remarkable differences; e.g., it is largely independent of the canonical IκB kinase (IKK) and even renders infected cells resistant to canonical NF-κB activation by the inflammatory cytokine TNF-α. Aberrant PRV-induced NF-κB activation may therefore paradoxically serve as a viral immune evasion strategy and may represent an important tool to unravel currently unknown mechanisms and consequences of NF-κB activation.

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Section: Discussionmentioning

confidence: 99%

Pseudorabies Virus Infection of Epithelial Cells Leads to Persistent but Aberrant Activation of the NF-κB Pathway, Inhibiting Hallmark NF-κB-Induced Proinflammatory Gene Expression

Romero

Waesberghe

Favoreel

2020

J Virol

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“…EBV in patients with IM leaves an enveloped antigen on the cell membrane, modifying it by penetrating B lymphocytes, which leads to activation of NK cells and cytotoxic T lymphocytes [18][19][20], and destruction of infected cells. As a result of cytolysis, cell degradation products enter the bloodstream, which are phagocyted by the means of neutrophilic granulocytes and macrophages.…”

Section: Discussionmentioning

confidence: 99%

Condition of Lipid Peroxide Oxidation and Antioxidant System in Patients With Infectious Mononucleosis

Shustval

Лядова

Volobueva

et al. 2018

The Journal of v. N. Karazin Kharkiv National University, Series "Medicine"

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The indicators of the activity of lipid peroxidation and the antioxidant system were studied in dynamics in 158 patients with infectious mononucleosis depending on the severity of the clinical course of the disease. It is proved that lipid peroxidation is significantly activated in patients with infectious mononucleosis as the severity of the disease increases and therefore increases the oxidative activity of blood plasma, the concentration of dyne conjugates and malondialdehyde in the blood, decreases the activity of antioxidant enzymes of erythrocytes (catalase, superoxide dismutase, glutathione peroxidase, glutathione reductase), glutathione peroxidase and glutathione reductase activity in plasma and lowering the concentration of total and reduced glutathione in the blood, as well as reduce the antioxidant activity of blood plasma and erythrocytes. Lipid peroxidation significantly increase and the activity of the antioxidant system decrease in patients with infectious mononucleosis in the acute period of the disease, as evidenced by the increased concentration of dyne conjugates, malonic dialdehyde and total oxidative plasma activity in the blood, reduced activity of the total antioxidant activity of plasma and erythrocytes, the decrease in the activity of antioxidant enzymes of erythrocytes catalase, superoxide dismutase, glutathione peroxidase, glutathione peroxidase and glutathione reductase of blood plasma, the decrease in the concentration of glutathione in the blood. The most pronounced disorders of lipid peroxidation and antioxidant system activity were found in patients with moderate-severe and severe infectious mononucleosis. The development of cytolytic syndrome in infectious mononucleosis is associated with the action of reactive oxygen forms species and lipid hydroperoxide.

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“…Since NF-κB can be activated downstream of CD40 and CD137, the expression of these two co-stimulators may play a role in the activation of NF-κB in EBV-T/NK cells. Honami Takada et al, demonstrates that EBV infection protects infected cells from apoptosis [23]. Cytidine deaminase (AID) acts as a DNA and RNA editor, its expression induces a genomic mutation that causes the development of B-cell lymphoma.…”

Section: Role Of Nk Cells In Ebv Controlmentioning

confidence: 99%

“…Cytidine deaminase (AID) acts as a DNA and RNA editor, its expression induces a genomic mutation that causes the development of B-cell lymphoma. Active NF-B in EBV T/NK cell line can lead to a positive regulation of AID which in turn can contribute to the induction of EBV [23].…”

Section: Role Of Nk Cells In Ebv Controlmentioning

confidence: 99%

NK/T Lymphocytes and LMP1: An Update on the Interactions and Mechanisms of Regulation

Ladkani¹

2018

VIJ

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Epstein-Barr virus (EBV) is a strictly human virus of the family of Herpesviridae. It infects almost the entire population; the infection is often asymptomatic and benign. However, many studies show that this virus can also participate in the oncogenesis of various human malignancies of epithelial or lymphocytic origin. After the primary infection, EBV remains latent in the body. During this latency, some proteins are expressed, including LMP1 (latent membrane protein). This protein, located at the membrane level, induces several signalling pathways involved in the survival of the host cell. It is described as the major oncoprotein of EBV. EBV-encoded latent membrane protein 1 is a multifunctional oncoprotein essential for transforming B lymphocytes into lymphoblastoid cell lines. The LMP1 gene, also referred to as BNLF1, encoding the LMP1 protein is relatively well conserved in its coding region, generally showing greater than 95% amino acid sequence identity between the different EBV isolates. NK cells appear to play an important role in the early control of EBV infection in both mice and humans. Few studies were interested in the interaction between LMP1 and NK and T cells. The aim of this review is to collect articles discussing the interaction between LMP1 and NK and T cells in order to describe the mechanisms of control of LMP1 by the NK/T cells and how LMP1 can regulate and promote them.

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Correction: EBV induces persistent NF-κB activation and contributes to survival of EBV-positive neoplastic T- or NK-cells

Cited by 11 publications

References 1 publication

Pseudorabies Virus Infection of Epithelial Cells Leads to Persistent but Aberrant Activation of the NF-κB Pathway, Inhibiting Hallmark NF-κB-Induced Proinflammatory Gene Expression

Pseudorabies Virus Infection of Epithelial Cells Leads to Persistent but Aberrant Activation of the NF-κB Pathway, Inhibiting Hallmark NF-κB-Induced Proinflammatory Gene Expression

Condition of Lipid Peroxide Oxidation and Antioxidant System in Patients With Infectious Mononucleosis

NK/T Lymphocytes and LMP1: An Update on the Interactions and Mechanisms of Regulation

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