Purpose. Herpes Simplex virus type 1 (HSV-1) is transmitted to the trigeminal ganglion (TG) of mice within 2 days of corneal infection, where it replicates briefly (2-9 days post infection [p.i.]) and then establishes a latent infection. The purpose of these studies was to identify the T cell populations that contribute to control of HSV-1 replication in the TG. Methods. Normal Balb/c mice, or Balb/c mice with a disrupted T cell receptor (TCR) α gene (αβ TCR null) were studied untreated or when depleted of γδ TCR+ cells by injection of the monoclonal antibody (GL3). At various times after HSV-1 corneal infection, the TG were excised and the presence of HSV antigens, T cells, and tumor necrosis factor (TNF) was evaluated by immunoperoxidase staining. Results. Normal mice showed an early accumulation of γδ TCR+ cells (days 3-7 p.i.), and a later infiltration of CD8+ cells (days 5-12 p.i.). Most of the CD8+ cells appeared to produce TNF, a cytokine that inhibits HSV-1 replication.. Depletion of γδ TCR+ cells from Balb/c mice enhanced early HSV-1 replication in the TG, but the virus was controlled by day 12 p.i. The αβ TCR null mice failed to control HSV-1 replication and died by day 30 p.i. Further depletion of γδ TCR+ cells from these mice enhanced early HSV-1 replication in the TG, and hastened death (day 15 p.i.). Conclusions. γδ TCR+ cells contribute to the control of acute HSV-1 replication in the TG, whereas CD8+ αβ TCR+ cells are required for complete eradication of replicating virus from the TG, and survival.
|Original language||English (US)|
|Journal||Investigative Ophthalmology and Visual Science|
|State||Published - Feb 15 1996|
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