scholarly journals Epstein–Barr Virus Infection of Pseudostratified Nasopharyngeal Epithelium Disrupts Epithelial Integrity

Cancers ◽  
2020 ◽  
Vol 12 (9) ◽  
pp. 2722
Author(s):  
Fenggang Yu ◽  
Yanan Lu ◽  
Yingying Li ◽  
Yuji Uchio ◽  
Utomo Andi Pangnguriseng ◽  
...  

Epstein–Barr virus (EBV) is a human oncogenic virus that causes several types of tumor, such as Burkitt’s lymphoma and nasopharyngeal carcinoma (NPC). NPC tumor cells are clonal expansions of latently EBV-infected epithelial cells. However, the mechanisms by which EBV transforms the nasopharyngeal epithelium is hampered, because of the lack of good in vitro model to pursue oncogenic process. Our primary nasopharyngeal epithelial cell cultures developed pseudostratified epithelium at the air-liquid interface, which was susceptible to EBV infection. Using the highly sensitive RNA in situ hybridization technique, we detected viral infection in diverse cell types, including ciliated cells, goblet cells, and basal cells. EBV-encoded small RNA-positive cells were more frequently detected in the suprabasal layer than in the basal layer. We established the most physiologically relevant EBV infection model of nasopharyngeal epithelial cells. This model will advance our understanding of EBV pathogenesis in the development of NPC.

Neoplasia ◽  
2006 ◽  
Vol 8 (3) ◽  
pp. 173-180 ◽  
Author(s):  
Angela Kwok Fung Lo ◽  
Kwok Wai Lo ◽  
Sai Wah Tsao ◽  
Hing Lok Wong ◽  
Jan Wai Ying Hui ◽  
...  

2020 ◽  
Vol 2 (1) ◽  
pp. 113-120
Author(s):  
Nur Suci Amanah

Nasopharyngeal carcinoma is a common disease in southern China. The etiologies of the main factors proposed for the pathogenesis of KNF include genetic factors, environmental factors and Epstein Barr Virus (EBV) infection. Other causes besides preserved food consumption include salted fish which have been involved in the etiology of NPC. The downward trend in the incidence of NPC has occurred in Hong Kong for the past 20 years, which is caused by changes in dietary habits. Despite the close relationship of EBV infection with NPC, the etiological role of EBV in the pathogenesis of NPC remains an interaction. EBV infection in primary nasopharyngeal epithelial cells occurs. Epstein Barr virus does not convert primary nasopharyngeal epithelial cells into proliferative clones, which is in sharp contrast to the well-documented ability of EBV to alter and perpetuate primary B cells. Genetic changes that are supported in the nasopharyngeal epithelium may be needed to support stable EBV infection. Non-viral factors as a cause of nasopharyngeal carcinoma still cannot be resolved with certainty. Non-viral factors are one of the risk factors that can increase the number of events arising from nasopharyngeal malignancies such as smoke, salted fish, formaldehyde, genetic, as soon as possible firewood, wood dust, chronic infection, throat protector, alcohol and traditional medicine.


2017 ◽  
Vol 372 (1732) ◽  
pp. 20160270 ◽  
Author(s):  
Sai Wah Tsao ◽  
Chi Man Tsang ◽  
Kwok Wai Lo

Epstein–Barr virus (EBV) is associated with multiple types of human cancer, including lymphoid and epithelial cancers. The closest association with EBV infection is seen in undifferentiated nasopharyngeal carcinoma (NPC), which is endemic in the southern Chinese population. A strong association between NPC risk and the HLA locus at chromosome 6p has been identified, indicating a link between the presentation of EBV antigens to host immune cells and NPC risk. EBV infection in NPC is clonal in origin, strongly suggesting that NPC develops from the clonal expansion of a single EBV-infected cell. In epithelial cells, the default program of EBV infection is lytic replication. However, latent infection is the predominant mode of EBV infection in NPC. The establishment of latent EBV infection in pre-invasive nasopharyngeal epithelium is believed to be an early stage of NPC pathogenesis. Recent genomic study of NPC has identified multiple somatic mutations in the upstream negative regulators of NF-κB signalling. Dysregulated NF-κB signalling may contribute to the establishment of latent EBV infection in NPC. Stable EBV infection and the expression of latent EBV genes are postulated to drive the transformation of pre-invasive nasopharyngeal epithelial cells to cancer cells through multiple pathways. This article is part of the themed issue ‘Human oncogenic viruses’.


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