The role of B cells and humoral immunity in herpes simplex virus (HSV) ocul
ar infections was studied in immunoglobulin IJ. chain gene-targeted B-cell-
deficient mice (mu K/O), At doses of virus well tolerated by immunocompeten
t mice, heightened susceptibility of mu K/O mice to herpetic encephalitis a
s well as to herpetic stromal keratitis (HSK) was observed. An explanation
was sought for the increased severity of HSK in the mu K/O mice. First, the
lack of antibody responses in mu K/O mice resulted in longer viral persist
ence and dissemination to the corneal stroma, the site of inflammation. Pro
longed virus expression in the corneal stroma was suggested to cause bystan
der activation of Th1-type CD4+ T cells, further contributing to the severi
ty of HSK lesion expression in mu K/O mice, Second, mu K/O mice generated m
inimal Th2 cytokine responses compared to wild-type mice, Such responses mi
ght serve to downregulate the severity of Th1-mediated HSR lesions.