Decreased vaginal disease in J-chain-deficient mice following herpes simplex type 2 genital infection

J-chain-deficient (Jch(-/-)) mice were used to study the role of polymeric IgA (plgA) in primary disease and protective immunity following genital her pes simplex type 2 (HSV-2) infection. Vaginal IgA in the Jch(-/-) mice was composed primarily of monomeric IgA and was not associated with secretory c omponent (SC). In contrast, vaginal IgA in wild-type (WT) mice was predomin antly polymeric and bound to SC. Following HSV-2 genital infection, the Jch (-/-) mice consistently exhibited fewer vaginal symptoms (P = 0.010) and mo rtality (P = 0.075) than did the WT mice. The variation in disease expressi on could not be explained by differences in local viral replication, since titers in vaginal wash fluid were comparable. To assess the effect of J cha in deficiency on protective immunity, WT and Jch(-/-) mice were immunized i ntravaginally with attenuated HSV-2, challenged intravaginally with wild-ty pe virus 5 weeks later, and evaluated for vaginal infection and neurologica l disease. Although the Jch(-/-) mice had reduced vaginal HSV-specific IgA and IgG levels following immunization, both WT and Jch(-/-) mice were prote cted from symptoms following wild-type virus challenge. We conclude that pl gA is not required for protective immunity against genital HSV-2 disease an d that J chain deficiency offers some protection against symptoms following primary HSV-2 genital infection. (C) 2000 Academic Press.