Distribution and phenotype of Epstein–Barr virus-infected cells in human pharyngeal tonsils

Hudnall, S. David; Ge, Yimin; Wei, Longxing; Yang, Ning; Wang, Hui Quin; Chen, Tiansheng

doi:10.1038/modpathol.3800369

Cited by 107 publications

(90 citation statements)

References 43 publications

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“…Although T and NK cells do not typically express CD21, it is expressed by thymic T cells [14]. In the tonsils of acute infectious mononucleosis patients, EBV-positive T and NK cells are seen, although they are rare [15,16]. In addition, T and NK cells are detected in the peripheral blood during acute infectious mononucleosis [17].…”

Section: Biology Of Ebv Infectionmentioning

confidence: 99%

Measuring Epstein–Barr virus (EBV) load: the significance and application for each EBV‐associated disease

Kimura

Ito

Suzuki

et al. 2008

Reviews in Medical Virology

137

144

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Because Epstein-Barr virus (EBV) is ubiquitous and persists latently in lymphocytes, simply detecting EBV is insufficient to diagnose EBV-associated diseases. Therefore, measuring the EBV load is necessary to diagnose EBVassociated diseases and to explore EBV pathogenesis. Due to the diverse biology of EBV, the significance of measuring EBV DNA and the optimal type of specimen differ among EBV-associated diseases. Recent advances in molecular technology have enabled the EBV genome to be quantitated rapidly and accurately. Real-time polymerase chain reaction (PCR) is a rapid and reliable method to quantify DNA and is widely used not only as a diagnostic tool, but also as a management tool for EBV-associated diseases. However, each laboratory currently measures EBV load with its own ''homebrew'' system, and there is no consensus on sample type, sample preparation protocol, or assay units. The EBV real-time PCR assay system must be standardised for large-scale studies and international comparisons.

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Section: Biology Of Ebv Infectionmentioning

confidence: 99%

Measuring Epstein–Barr virus (EBV) load: the significance and application for each EBV‐associated disease

Kimura

Ito

Suzuki

et al. 2008

Reviews in Medical Virology

137

144

View full text Add to dashboard Cite

show abstract

“…Although EBV replication has been detected in occasional tonsillar crypt B lymphocytes (1,11,26,27), it is uncertain if so few cells can account for the high levels of virus often detected in saliva (19,42). EBV transition into oral epithelium via pre-LC and subsequent replication at multiple oral epithelial foci would serve as a viral production amplifier, achieving greater quantities in saliva and more efficient transmission.…”

Section: Cd11cmentioning

confidence: 99%

Epstein-Barr Virus Infection of Langerhans Cell Precursors as a Mechanism of Oral Epithelial Entry, Persistence, and Reactivation

Walling

Ray²,

Nichols

et al. 2007

J Virol

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Epstein-Barr virus (EBV) is a ubiquitous human herpesvirus associated with many malignant and nonmalignant human diseases. Life-long latent EBV persistence occurs in blood-borne B lymphocytes, while EBV intermittently productively replicates in mucosal epithelia. Although several models have previously been proposed, the mechanism of EBV transition between these two reservoirs of infection has not been determined. In this study, we present the first evidence demonstrating that EBV latently infects a unique subset of blood-borne mononuclear cells that are direct precursors to Langerhans cells and that EBV both latently and productively infects oral epithelium-resident cells that are likely Langerhans cells. These data form the basis of a proposed new model of EBV transition from blood to oral epithelium in which EBV-infected Langerhans cell precursors serve to transport EBV to the oral epithelium as they migrate and differentiate into oral Langerhans cells. This new model contributes fresh insight into the natural history of EBV infection and the pathogenesis of EBV-associated epithelial disease. Epstein-Barr virus (EBV) is a human herpesvirus that ultimately infects 95% of adults worldwide. EBV is transmitted via mucosal fluids and establishes life-long persistent infection.Although persistent infection is asymptomatic in most people, EBV is associated with benign syndromes, including infectious mononucleosis and oral hairy leukoplakia, and a wide variety of both lymphoid and mucosal epithelial malignancies. Persistent latent EBV infection occurs in memory B lymphocytes that circulate in blood (22). While latent EBV infection also occurs in some epithelial malignancies (29), EBV infection of epithelial cells typically results in productive replication, as demonstrated in oral hairy leukoplakia (9) and in normal oral epithelium (8,10,48).Three different models have previously been proposed to explain the transition of EBV from the latent reservoir of infection in blood-borne B lymphocytes to sites of productive replication in oral epithelium. Model 1 proposes that B lymphocytes carrying latent EBV infection migrate from the blood to the epithelium, where the EBV reactivates and infects adjacent epithelial cells (12), but evidence of intraepithelial B lymphocytes in normal oral epithelium or in oral hairy leukoplakia is lacking (30, 33). Model 2 proposes that EBV virions produced by B lymphocytes in the oral submucosa bind submucosal EBV-specific dimeric immunoglobulin A (IgA) and enter basal oral epithelial cells by endocytosis via the polymeric Ig receptor (37), but the polymeric Ig receptor is not expressed in oral epithelium (23). Model 3 proposes that EBV virions produced by B lymphocytes in oral lymphoid tissues (26) gain access to and infect middle-and upper-layer oral epithelial cells as a result of microscopic traumatic epithelial injury, such as that which occurs during mastication. However, this model is contradicted by evidence that EBV transitions into oral epithelium as cell-associated latent infecti...

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“…For instance, it is unknown if type II and III NPCs have similar or different EBV etiologies. An important step forward was the discovery of EBV in healthy nasopharyngeal epithelial cells (10,11), indicating that EBV may be present at the initial stages of NPC development. However, NPCs originate from translational and crypt epithelial from the lateral wall of the nasopharynx ( fossa of Rosenmuller).…”

Section: Introductionmentioning

confidence: 99%

IFN-α–Stimulated Genes and Epstein-Barr Virus Gene Expression Distinguish WHO Type II and III Nasopharyngeal Carcinomas

et al. 2007

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Nonkeratinizing nasopharyngeal carcinoma (NPC) is 100% associated with Epstein-Barr Virus (EBV) and divided into two subtypes (WHO types II and III) based on histology. We tested whether these subtypes can be distinguished at the molecular genetic level using an algorithm that analyzes sets of related genes (gene set enrichment analysis). We found that a class of IFN-stimulated genes (ISG), frequently associated with the antiviral response, was significantly activated in type III versus type II NPC. Consistent with this, replication of the endogenous EBV was suppressed in type III. A strong association was also seen with a subset of ISGs previously identified in systemic lupus erythematosus, another disease in which 'normal' EBV biology is deregulated, suggesting that this pattern of ISG expression may be linked to the increased EBV activity in both diseases. In contrast, unsupervised hierarchical clustering of the complete expression profiles failed to distinguish the two subsets. These results suggest that type II and III NPC have not originated from obviously distinct epithelial precursors; rather, the histologic differences may be a consequence of a differential antiviral response, involving IFNs, to chronic EBV infection. [Cancer Res 2007;67(2):474-81]

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Distribution and phenotype of Epstein–Barr virus-infected cells in human pharyngeal tonsils

Cited by 107 publications

References 43 publications

Measuring Epstein–Barr virus (EBV) load: the significance and application for each EBV‐associated disease

Measuring Epstein–Barr virus (EBV) load: the significance and application for each EBV‐associated disease

Epstein-Barr Virus Infection of Langerhans Cell Precursors as a Mechanism of Oral Epithelial Entry, Persistence, and Reactivation

IFN-α–Stimulated Genes and Epstein-Barr Virus Gene Expression Distinguish WHO Type II and III Nasopharyngeal Carcinomas

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