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Epstein-Barr Virus (EBV) and Nasopharyngeal Carcinoma (NPC): Pathogenesis, Viral-Host Interaction...
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Epstein-Barr Virus (EBV) and Nasopharyngeal Carcinoma (NPC): Pathogenesis, Viral-Host Interaction and Therapeutic Strategies

A special issue of Pathogens (ISSN 2076-0817). This special issue belongs to the section "Viral Pathogens".

Deadline for manuscript submissions: closed (1 October 2021) | Viewed by 11623

Special Issue Editor

Dr. Chi Man Tsang

E-Mail Website
Guest Editor
Department of Anatomical and Cellular Pathology, The Chinese University of Hong Kong, Hong Kong SAR, China
Interests: nasopharyngeal carcinoma; Epstein–Barr virus; translational research
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Epstein–Barr virus (EBV) was discovered in 1964 and is now recognized as a founding member of the human tumor viruses. In particular, it is nearly 100% associated with undifferentiated nasopharyngeal carcinoma (NPC), which is a lymphocyte-rich epithelial tumor arising from nasopharyngeal mucosa. The strong causal relationship between EBV infection and NPC development has been well-established by the presence of a clonal EBV genome in NPC and precancerous lesions, and the evidence of various viral products in promoting carcinogenesis, invasion, and immunoevasion for NPC progression. However, despite decades of investigation, the interaction of EBV with host and stromal cells in affecting and transforming the normal nasopharyngeal epithelial cells to cancerous cells is not completely understood, and the development of EBV-specific therapeutic strategies to treat this associated cancer is still a major challenge.

This Special Issue is devoted to highlight and identify new findings underlying the EBV-mediated pathogenesis in NPC and the translational opportunities in developing novel EBV-targeting interventions. It also focuses on expanding upon the current body of knowledge with new insights on viral interaction with the host and stromal cells in the tumor microenvironment. We welcome submissions of original research and review manuscripts that cover any aspects within EBV persistence, invasion, immunoevasion, carcinogenesis, and development of additional therapeutic options in treating the disease.

Dr. Chi Man Tsang
Guest Editor

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Keywords

  • EBV infection
  • EBV persistence
  • pathogenesis of NPC
  • invasion
  • immunoinvasion
  • viral interaction
  • translational study
  • therapeutic intervention

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Published Papers (3 papers)

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Research

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12 pages, 7005 KiB  
Article
Epstein-Barr Virus Promotes Tumor Angiogenesis by Activating STIM1-Dependent Ca2+ Signaling in Nasopharyngeal Carcinoma
by Jiaxiang Ye, Jiazhang Wei, Yue Luo, Yayan Deng, Ting Que, Xiaojian Zhang, Fei Liu, Jinyan Zhang and Xiaoling Luo
Pathogens 2021, 10(10), 1275; https://doi.org/10.3390/pathogens10101275 - 3 Oct 2021
Cited by 8 | Viewed by 2768
Abstract
Epstein-Barr virus (EBV) promotes tumor angiogenesis in nasopharyngeal carcinoma (NPC) by activating store-operated Ca2+ entry. Since such entry has been linked to stromal interaction molecule 1 (STIM1), we examined whether the virus acts via STIM1-dependent Ca2+ signaling to promote tumor angiogenesis [...] Read more.
Epstein-Barr virus (EBV) promotes tumor angiogenesis in nasopharyngeal carcinoma (NPC) by activating store-operated Ca2+ entry. Since such entry has been linked to stromal interaction molecule 1 (STIM1), we examined whether the virus acts via STIM1-dependent Ca2+ signaling to promote tumor angiogenesis in NPC. STIM1 expression was detected in NPC cell lines HK1 and CNE2 that were negative or positive for EBV. STIM1 was knocked down in EBV-positive cells using recombinant lentivirus, then cytosolic Ca2+ levels were measured based on fluorescence resonance energy transfer. Cells were also exposed to epidermal growth factor (EGF), and secretion of vascular endothelial growth factor (VEGF) was measured using an enzyme-linked immunosorbent assay. Endothelial tube formation was quantified in an in vitro angiogenesis assay. Growth of CNE2-EBV xenografts was measured in mice, and angiogenesis was assessed based on immunohistochemical staining against CD31. Paraffin-embedded NPC tissues from patients were assayed for CD31 and STIM1. EGFR and ERK signaling pathways were assessed in NPC cell lines. STIM1 expression was higher in EBV-positive than in EBV-negative NPC cell lines. STIM1 knockdown in EBV-positive NPC cells significantly reduced Ca2+ influx and VEGF production after EGF treatment. STIM1 knockdown also inhibited xenograft growth and angiogenesis. Moreover, CD31 expression level was higher in EBV-positive than EBV-negative NPC tissues, and high expression of CD31 co-localized with high expression of STIM1 in EBV-positive tissues from NPC patients. Viral infection of NPC cells led to higher levels of phosphorylated ERK1/2 after EGF treatment, which STIM1 knockdown partially reversed. Our results suggest that EBV promotes EGF-induced ERK1/2 signaling by activating STIM1-dependent Ca2+ signaling, and that blocking such signaling may inhibit EBV-promoted angiogenesis in NPC. Full article
(This article belongs to the Special Issue Epstein-Barr Virus (EBV) and Nasopharyngeal Carcinoma (NPC): Pathogenesis, Viral-Host Interaction and Therapeutic Strategies)
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Review

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17 pages, 1036 KiB  
Review
Nasopharyngeal Carcinoma: The Role of the EGFR in Epstein–Barr Virus Infection
by Xintong Peng, Yanling Zhou, Yongguang Tao and Shuang Liu
Pathogens 2021, 10(9), 1113; https://doi.org/10.3390/pathogens10091113 - 31 Aug 2021
Cited by 18 | Viewed by 4207
Abstract
Epstein–Barr virus (EBV), a type 4 γ herpes virus, is recognized as a causative agent in nasopharyngeal carcinoma (NPC). Incidence of EBV-positive NPC have grown in recent decades along with worse outcomes compared with their EBV-negative counterparts. Latent membrane protein 1 (LMP1), encoded [...] Read more.
Epstein–Barr virus (EBV), a type 4 γ herpes virus, is recognized as a causative agent in nasopharyngeal carcinoma (NPC). Incidence of EBV-positive NPC have grown in recent decades along with worse outcomes compared with their EBV-negative counterparts. Latent membrane protein 1 (LMP1), encoded by EBV, induces NPC progression. The epidermal growth factor receptor (EGFR), a member of the ErbB family of receptor tyrosine kinases (RTK), is a driver of tumorigenesis, including for NPC. Little data exist on the relationship between EGFR and EBV-induced NPC. In our initial review, we found that LMP1 promoted the expression of EGFR in NPC in two main ways: the NF-κB pathway and STAT3 activation. On the other hand, EGFR also enhances EBV infection in NPC cells. Moreover, activation of EGFR signalling affects NPC cell proliferation, cell cycle progression, angiogenesis, invasion, and metastasis. Since EGFR promotes tumorigenesis and progression by downstream signalling pathways, causing poor outcomes in NPC patients, EGFR-targeted drugs could be considered a newly developed anti-tumor drug. Here, we summarize the major studies on EBV, EGFR, and LMP1-regulatory EGFR expression and nucleus location in NPC and discuss the clinical efficacy of EGFR-targeted agents in locally advanced NPC (LA NPC) and recurrent or metastatic NPC (R/M NPC) patients. Full article
(This article belongs to the Special Issue Epstein-Barr Virus (EBV) and Nasopharyngeal Carcinoma (NPC): Pathogenesis, Viral-Host Interaction and Therapeutic Strategies)
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Other

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31 pages, 9358 KiB  
Systematic Review
A Systematic Review of Epstein–Barr Virus Latent Membrane Protein 1 (LMP1) Gene Variants in Nasopharyngeal Carcinoma
by Ana Banko, Danijela Miljanovic, Ivana Lazarevic and Andja Cirkovic
Pathogens 2021, 10(8), 1057; https://doi.org/10.3390/pathogens10081057 - 20 Aug 2021
Cited by 10 | Viewed by 3507
Abstract
Nasopharyngeal carcinoma (NPC) is an aggressive tumor with a complex etiology. Although Epstein–Barr virus (EBV) infection is known environmental factor for NPC development, the degree to which EBV naturally infects nasopharyngeal epithelium and the moment when and why the virus actively begins to [...] Read more.
Nasopharyngeal carcinoma (NPC) is an aggressive tumor with a complex etiology. Although Epstein–Barr virus (EBV) infection is known environmental factor for NPC development, the degree to which EBV naturally infects nasopharyngeal epithelium and the moment when and why the virus actively begins to affect cell transformation remains questionable. The aim of this study was to explore the association between LMP1 gene variability and potential contribution to NPC development. A systematic review was performed through searches of PubMed, Web of Science (WoS) and SCOPUS electronic databases. Additionally, meta-analysis of the difference in the frequency of seven LMP1 gene variants in NPC and control individuals was accomplished. The results from this study give a proof of concept for the association between 30 bp deletion (OR = 3.53, 95% CI = 1.48–8.43) and Xhol loss (OR = 14.17, 95% CI = 4.99–40.20) and NPC susceptibility when comparing biopsies from NPC and healthy individuals. Otherwise, 30 bp deletion from NPC biopsies could not distinguish NPC from EBV-associated non-NPC tumors (OR = 1.74, 95% CI = 0.81–3.75). However, B95-8, China1 and North Carolina variants were uncommon for NPC individuals. Much more efforts remains to be done to verify the biological significance of the differences observed, define so-called “high-risk” EBV variants and make it available for clinical application. Full article
(This article belongs to the Special Issue Epstein-Barr Virus (EBV) and Nasopharyngeal Carcinoma (NPC): Pathogenesis, Viral-Host Interaction and Therapeutic Strategies)
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