Prenatal transfer of low amounts of herpes simplex virus (HSV)-specific antibody protects newborn mice against HSV infection during acute maternal stress.

Given their immunocompromised status, neonates rely heavily upon maternally derived, herpes simplex virus (HSV)-specific antibody for resistance to HSV infection. Interestingly, previous studies have documented a decreased transfer of maternal IgG antibody and immunocompetence of the offspring following perinatal exposure to stress-induced corticosterone. However, we recently demonstrated that the transplacental transfer of relatively high amounts of HSV-specific antibody is resilient to acute maternal stress and protects neonatal mice against HSV-2-associated mortality. Our current studies demonstrate that transplacentally acquired, HSV-specific antibody declines rapidly in neonate serum such that by day 7 postnatal only 10% of this antibody remains. Prenatal stress does not affect the overall kinetics with which the HSV-specific antibody declines. Surprisingly, this relatively low level of antibody is still sufficient to protect 7-day-old mice against HSV-associated mortality. To extend these studies, we utilized an immunization strategy that elicits low levels of HSV-specific antibody in maternal serum. We demonstrated that despite a stress-induced increase in corticosterone, the prenatal transfer and protective capacity of low amounts of HSV-specific antibody remains intact during acute maternal stress.