HSV-1 retinitis and delayed hypersensitivity in DBA/2 and C57BL/6 mice.

Following uniocular anterior chamber (a.c.) inoculation of HSV-1 into BALB/c mice, the architecture of the uninoculated eye is destroyed by a pan-retinal inflammatory process within 10 days. BALB/c inoculated with HSV-1 via the a.c. route also develop anterior chamber associated immune deviation (ACAID), one characteristic of which is impairment of virus-specific delayed hypersensitivity (DH) responsiveness. To determine whether other strains of mice develop ACAID and contralateral retinitis, DBA/2 and C57BL/6 mice were inoculated with HSV-1 (KOS strain) via the a.c. route. At intervals after inoculation, animals were examined clinically for evidence of retinitis in the uninoculated eye and were either (1) sacrificed for virus recovery studies or (2) ear-challenged for DH assays. Seven of 15 DBA/2 mice had clinical evidence of retinitis in the uninoculated eye by day 10 post-inoculation (p.i.). At this time, the average titer of virus in the uninoculated eyes was 3.37 log10 PFU/ml. Animals of this strain also had significantly impaired HSV-1 virus-specific DH responses consistent with ACAID. No (0/12) C57BL/6 developed contralateral retinitis; at day 10 p.i., the average virus titer in the uninoculated eyes of C57BL/6 mice was 1.10 log10 PFU/ml. Following a.c. inoculation of HSV-1, C57BL/6 mice developed vigorous DH responses comparable to those of subcutaneously immunized, DH-positive animals. The results of these experiments suggest that different strains of mice vary in their susceptibility to HSV-1 retinitis and that the development of retinitis is linked to the amount of virus in the uninoculated eye.(ABSTRACT TRUNCATED AT 250 WORDS)