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J Virol. 2015 Oct;89(19):10110-4. doi: 10.1128/JVI.01110-15. Epub 2015 Jul 15.

Latent Expression of the Epstein-Barr Virus (EBV)-Encoded Major Histocompatibility Complex Class I TAP Inhibitor, BNLF2a, in EBV-Positive Gastric Carcinomas.

Author information

1
Department of Pathology, Tulane University Health Sciences Center, New Orleans, Louisiana, USA Tulane Cancer Center, New Orleans, Louisiana, USA.
2
Department of Microbiology, Immunology & Parasitology, Louisiana State University School of Medicine, New Orleans, Louisiana, USA.
3
Department of Biostatistics and Bioinformatics, Tulane University Health Sciences Center, New Orleans, Louisiana, USA.
4
Department of Pathology, Tulane University Health Sciences Center, New Orleans, Louisiana, USA.
5
Tulane Cancer Center, New Orleans, Louisiana, USA Department of Pulmonary Diseases, Critical Care, and Environmental Medicine, Tulane University Health Sciences Center, New Orleans, Louisiana, USA.
6
Department of Pathology, Tulane University Health Sciences Center, New Orleans, Louisiana, USA Tulane Cancer Center, New Orleans, Louisiana, USA erik@tulane.edu.

Abstract

The Epstein-Barr virus (EBV) BNLF2a gene product provides immune evasion properties to infected cells through inhibition of transporter associated with antigen processing (TAP)-mediated transport of antigen peptides. Although BNLF2a is considered to be a lytic gene, we demonstrate that it is expressed in nearly half of the EBV-associated gastric carcinomas analyzed. Further, we show that BNLF2a expression is dissociated from lytic gene expression. BNLF2a is therefore expressed in this latency setting, potentially helping protect the infected tumor cells from immunosurveillance.

PMID:
26178981
PMCID:
PMC4577887
DOI:
10.1128/JVI.01110-15
[Indexed for MEDLINE]
Free PMC Article

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