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Publication Details
AFRICAN RESEARCH NEXUS
SHINING A SPOTLIGHT ON AFRICAN RESEARCH
agricultural and biological sciences
The herpes simplex virus 1 latency-associated transcript promotes functional exhaustion of virus-specific CD8
+
T cells in latently infected trigeminal ganglia: A novel immune evasion mechanism
Journal of Virology, Volume 85, No. 17, Year 2011
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Description
Following ocular herpes simplex virus 1 (HSV-1) infection of C57BL/6 mice, HSV-specific (HSV-gB 498-505 tetramer +) CD8 + T cells are induced, selectively retained in latently infected trigeminal ganglia (TG), and appear to decrease HSV-1 reactivation. The HSV-1 latency-associated transcript (LAT) gene, the only viral gene that is abundantly transcribed during latency, increases reactivation. Previously we found that during latency with HSV-1 strain McKrae-derived viruses, more of the total TG resident CD8 T cells expressed markers of exhaustion with LAT + virus compared to LAT - virus. Here we extend these findings to HSV-1 strain 17syn+-derived LAT + and LAT - viruses and to a virus expressing just the first 20% of LAT. Thus, the previous findings were not an artifact of HSV-1 strain McKrae, and the LAT function involved mapped to the first 1.5 kb of LAT. Importantly, to our knowledge, we show here for the first time that during LAT + virus latency, most of the HSV-1-specific TG resident CD8 T cells were functionally exhausted, as judged by low cytotoxic function and decreased gamma interferon (IFN-γ) and tumor necrosis factor alpha (TNF-α) production. This resulted in LAT - TG having more functional HSV-gB 498-505 tetramer + CD8 + T cells compared to LAT + TG. In addition, LAT expression, in the absence of other HSV-1 gene products, appeared to be able to directly or indirectly upregulate both PD-L1 and major histocompatibility complex class I (MHC-I) on mouse neuroblastoma cells (Neuro2A). These findings may constitute a novel immune evasion mechanism whereby the HSV-1 LAT directly or indirectly promotes functional exhaustion (i.e., dysfunction) of HSVspecific CD8 + T cells in latently infected TG, resulting in increased virus reactivation. © 2011, American Society for Microbiology.
Authors & Co-Authors
Chentoufi, Aziz Alami
United States, Irvine
Uci School of Medicine
Saudi Arabia, Riyadh
King Fahad Medical City
Kritzer, Elizabeth
United States, Irvine
Uci School of Medicine
Tran, Michael V.
United States, Irvine
Uci School of Medicine
Dasgupta, Gargi
United States, Irvine
Uci School of Medicine
Lim, Chang Hyun
United States, Irvine
Uci School of Medicine
Yu, David C.
United States, Irvine
Uci School of Medicine
Afifi, Rasha E.
United States, Irvine
Uci School of Medicine
Jiang, Xianzhi
United States, Irvine
Uci School of Medicine
Carpenter, Dale
United States, Irvine
Uci School of Medicine
Osorio, Nelson
United States, Irvine
Uci School of Medicine
Hsiang, Chinhui
United States, Irvine
Uci School of Medicine
Nesburn, Anthony B.M.D.
United States, Irvine
Uci School of Medicine
Wechsler, Steven L.
United States, Irvine
Uci School of Medicine
United States, Irvine
University of California, Irvine
BenMohamed, Lbachir
United States, Irvine
Uci School of Medicine
United States, Orange
Uci Medical Center
Statistics
Citations: 74
Authors: 14
Affiliations: 4
Identifiers
Doi:
10.1128/JVI.00587-11
ISSN:
0022538X
e-ISSN:
10985514
Research Areas
Cancer
Genetics And Genomics