Ocular herpes simplex virus infection is diminished by depletion of B lymphocytes.

Abstract

Rabbit anti-mouse mu-chain serum was used to deplete specifically IgM-bearing B cells and B cell function in BALB/c mice. B cell-depleted and normal littermates were infected via the cornea with herpes simplex virus type 1 (HSV-1) at 4 to 5 wk of age. B cell-depleted mice had a reduced number of lymphocytes bearing surface immunoglobulin and a greatly reduced ability to produce antibody. Mortality was reduced from 89% in normal controls to 42% in B cell-depleted mice (p less than 0.001) and peak virus shedding from eyes was also reduced as much as 90% in the B cell-depleted mice (p less than or equal to 0.0005). These results support the hypothesis that a B cell function of normal mice somehow contributes directly or indirectly to the enhanced mortality of mice infected with HSV.

Antiviral CD19+CD27+Memory B Cells Are Associated with Protection from Recurrent Asymptomatic Ocular Herpesvirus Infection

“…Reports indicate that high titers of herpes-neutralizing antibodies in the blood of symptomatic herpes is neither associated with the frequency of symptomatic herpes (31,32) nor protection after vaccination (30,33). Thus, the general understanding is that although anti-herpes antibodies are neutralizing or binding, they are not protective (34,35). Another theory states that certain HSV-specific antibodies may function protectively in tissue near the site of viral release.…”

“…Memory B cells can survive for long periods and can induce faster and stronger humoral responses when they reencounter the same antigen (34), in contrast to plasma cells, which provide the first line of protection against infection but do not respond to the second infection because of low expression of membrane-bound Ig (35). There is evidence that indicates that human memory B cells reside mostly in the spleen, and some memory B cells recirculate in the blood.…”