FIG. 4.

Infection with replication-defective HSV (UL6 positive or negative) fails to induce HSK in SCID mice reconstituted with HSV immune T cells. SCID mice (n = 5/group) were infected with ICP4^−/−, ICP8^−/−, and HSV-1 KOS (5 × 10⁵ PFU) on scarified corneas at days 0, 2, and 4. At day 1 postinfection, SCID mice were reconstituted with 10⁷ HSV immune splenocytes in a 400-μl volume of 1× PBS given i.v. The data represents the results from one of two independent experiments with similar results. (A) Mean clinical scores of SCID mice at days 7, 9, 11, and 12 postinfection. Mice were scored by using a slit-lamp microscope as described in Materials and Methods. (B and C) Mice were terminated at day 13 postinfection, and cervical and submandibular DLN cells were used as responders in an HSV-specific lymphoproliferation assay (C) or were stained for activation markers CD62L, CD45 RB, and CD44 by flow cytometry assay (B) as described in Materials and Methods. The percentage of cell surface expression of activation markers under marker M2 is indicated in the histograms. The data indicate the presence of activated HSV-specific CD4⁺ T cells in all of the wild-type and mutant virus-infected reconstituted SCID mice groups irrespective of the development of HSK lesions shown in panel A.