A CD8+ T cell immune evasion protein specific to Epstein-Barr virus and its close relatives in Old World primates Export

@article{citeulike:2749454, abstract = {{gamma} 1-Herpesviruses such as Epstein-Barr virus (EBV) have a unique ability to amplify virus loads in vivo through latent growth-transforming infection. Whether they, like {alpha}- and {beta}-herpesviruses, have been driven to actively evade immune detection of replicative (lytic) infection remains a moot point. We were prompted to readdress this question by recent work (Pudney, V.A., A.M. Leese, A.B. Rickinson, and A.D. Hislop. 2005. J. Exp. Med. 201:349-360; Ressing, M.E., S.E. Keating, D. van Leeuwen, D. Koppers-Lalic, I.Y. Pappworth, E.J.H.J. Wiertz, and M. Rowe. 2005. J. Immunol. 174:6829-6838) showing that, as EBV-infected cells move through the lytic cycle, their susceptibility to EBV-specific CD8+ T cell recognition falls dramatically, concomitant with a reductions in transporter associated with antigen processing (TAP) function and surface human histocompatibility leukocyte antigen (HLA) class I expression. Screening of genes that are unique to EBV and closely related {gamma}1-herpesviruses of Old World primates identified an early EBV lytic cycle gene, BNLF2a, which efficiently blocks antigen-specific CD8+ T cell recognition through HLA-A-, HLA-B-, and HLA-C-restricting alleles when expressed in target cells in vitro. The small (60-amino acid) BNLF2a protein mediated its effects through interacting with the TAP complex and inhibiting both its peptide- and ATP-binding functions. Furthermore, this targeting of the major histocompatibility complex class I pathway appears to be conserved among the BNLF2a homologues of Old World primate {gamma}1-herpesviruses. Thus, even the acquisition of latent cycle genes endowing unique growth-transforming ability has not liberated these agents from evolutionary pressure to evade CD8+ T cell control over virus replicative foci. 10.1084/jem.20070256}, author = {Hislop, Andrew D. and Ressing, Maaike E. and van Leeuwen, Daphne and Pudney, Victoria A. and Horst, Danielle and Koppers-Lalic, Danijela and Croft, Nathan P. and Neefjes, Jacques J. and Rickinson, Alan B. and Wiertz, Emmanuel J.}, citeulike-article-id = {2749454}, citeulike-linkout-0 = {http://dx.doi.org/10.1084/jem.20070256}, citeulike-linkout-1 = {http://www.jem.org/cgi/content/abstract/204/8/1863}, citeulike-linkout-2 = {http://view.ncbi.nlm.nih.gov/pubmed/17620360}, citeulike-linkout-3 = {http://www.hubmed.org/display.cgi?uids=17620360}, day = {6}, doi = {10.1084/jem.20070256}, journal = {J. Exp. Med.}, keywords = {ctl, ebv, virus}, month = {August}, number = {8}, pages = {1863--1873}, posted-at = {2008-05-03 18:55:55}, priority = {4}, title = {A CD8+ T cell immune evasion protein specific to Epstein-Barr virus and its close relatives in Old World primates}, url = {http://dx.doi.org/10.1084/jem.20070256}, volume = {204}, year = {2007} }

TY - JOUR ID - citeulike:2749454 L3 - citeulike-article-id:2749454 N2 - {gamma} 1-Herpesviruses such as Epstein-Barr virus (EBV) have a unique ability to amplify virus loads in vivo through latent growth-transforming infection. Whether they, like {alpha}- and {beta}-herpesviruses, have been driven to actively evade immune detection of replicative (lytic) infection remains a moot point. We were prompted to readdress this question by recent work (Pudney, V.A., A.M. Leese, A.B. Rickinson, and A.D. Hislop. 2005. J. Exp. Med. 201:349-360; Ressing, M.E., S.E. Keating, D. van Leeuwen, D. Koppers-Lalic, I.Y. Pappworth, E.J.H.J. Wiertz, and M. Rowe. 2005. J. Immunol. 174:6829-6838) showing that, as EBV-infected cells move through the lytic cycle, their susceptibility to EBV-specific CD8+ T cell recognition falls dramatically, concomitant with a reductions in transporter associated with antigen processing (TAP) function and surface human histocompatibility leukocyte antigen (HLA) class I expression. Screening of genes that are unique to EBV and closely related {gamma}1-herpesviruses of Old World primates identified an early EBV lytic cycle gene, BNLF2a, which efficiently blocks antigen-specific CD8+ T cell recognition through HLA-A-, HLA-B-, and HLA-C-restricting alleles when expressed in target cells in vitro. The small (60-amino acid) BNLF2a protein mediated its effects through interacting with the TAP complex and inhibiting both its peptide- and ATP-binding functions. Furthermore, this targeting of the major histocompatibility complex class I pathway appears to be conserved among the BNLF2a homologues of Old World primate {gamma}1-herpesviruses. Thus, even the acquisition of latent cycle genes endowing unique growth-transforming ability has not liberated these agents from evolutionary pressure to evade CD8+ T cell control over virus replicative foci. 10.1084/jem.20070256 IS - 8 JF - J. Exp. Med. EP - 1873 TI - A CD8+ T cell immune evasion protein specific to Epstein-Barr virus and its close relatives in Old World primates VL - 204 SP - 1863 KW - ctl KW - ebv KW - virus AU - Hislop, Andrew AU - Ressing, Maaike AU - van Leeuwen, Daphne AU - Pudney, Victoria AU - Horst, Danielle AU - Koppers-Lalic, Danijela AU - Croft, Nathan AU - Neefjes, Jacques AU - Rickinson, Alan AU - Wiertz, Emmanuel PY - 2007/08/06/ UR - http://dx.doi.org/10.1084/jem.20070256 ER -