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Reevaluating the CD8 T-cell response to herpes simplex virus type 1: involvement of CD8 T cells reactive to subdominant epitopes.

TitleReevaluating the CD8 T-cell response to herpes simplex virus type 1: involvement of CD8 T cells reactive to subdominant epitopes.
Publication TypeJournal Article
Year of Publication2009
AuthorsSheridan BS, Cherpes TL, Urban J, Kalinski P, Hendricks RL
JournalJ Virol
Volume83
Issue5
Pagination2237-45
Date Published2009 Mar
ISSN1098-5514
KeywordsAnimals, Antigens, Viral, CD8-Positive T-Lymphocytes, Cells, Cultured, Epitopes, T-Lymphocyte, Female, Herpes Simplex, Herpesvirus 1, Human, Interferon-gamma, Lymphocyte Activation, Mice, Mice, Inbred C57BL, Trigeminal Ganglion, Viral Envelope Proteins, Virus Latency
Abstract

<p>In C57BL/6 (B6) mice, most herpes simplex virus (HSV)-specific CD8 T cells recognize a strongly immunodominant epitope on glycoprotein B (gB498) and can inhibit HSV type 1 (HSV-1) reactivation from latency in trigeminal ganglia (TG). However, half of the CD8 T cells retained in latently infected TG of B6 mice are not gB498 specific and have been largely ignored. The following observations from our current study indicate that these gB498-nonspecific CD8 T cells are HSV specific and may contribute to the control of HSV-1 latency. First, following corneal infection, OVA257-specific OT-1 CD8 T cells do not infiltrate the infected TG unless mice are simultaneously immunized with OVA257 peptide, and then they are not retained. Second, 30% of CD8 T cells in acutely infected TG that produce gamma interferon in response to HSV-1 stimulation directly ex vivo are gB498 nonspecific, and these cells maintain an activation phenotype during viral latency. Finally, gB498-nonspecific CD8 T cells are expanded in ex vivo cultures of latently infected TG and inhibit HSV-1 reactivation from latency in the absence of gB498-specific CD8 T cells. We conclude that many of the CD8 T cells that infiltrate and are retained in infected TG are HSV specific and potentially contribute to maintenance of HSV-1 latency. Identification of the viral proteins recognized by these cells will contribute to a better understanding of the dynamics of HSV-1 latency.</p>

DOI10.1128/JVI.01699-08
Alternate JournalJ. Virol.
Citation KeyCK98
PubMed ID19073721
PubMed Central IDPMC2643732
Grant ListT32 AI060525 / AI / NIAID NIH HHS / United States
T32-AI060525 / AI / NIAID NIH HHS / United States
R01 EY005945 / EY / NEI NIH HHS / United States
R01-EY05945 / EY / NEI NIH HHS / United States
P30-EY08098 / EY / NEI NIH HHS / United States
K23 AI064396 / AI / NIAID NIH HHS / United States
K23-AI064396 / AI / NIAID NIH HHS / United States
P30 EY008098 / EY / NEI NIH HHS / United States