In adults, psychological stress regulates immune responsiveness in part via the increased levels of corticosterone that are produced as a result of hypothalamic-pituitary-adrenal (HPA) axis activation. However, there is a lack of knowledge as to the role such regulation may play in the neonate. Neonates are severely compromised in their ability to generate an immune response to pathogens encountered after birth and therefore rely heavily on maternally derived antibody acquired postnatally through the milk. This passive transfer of antibody is critical for protection of the neonate from severe herpes simplex virus (HSV) infection and mortality. Using a well-established postnatal restraint/light stress model, we determined whether maternal stress and the associated increases in corticosterone would affect the transmammary transfer of antibody and subsequent neonate susceptibility to HSV-associated mortality. Serum corticosterone levels were markedly increased in lactating mice subjected to the restraint/light stress, and increased levels of corticosterone were transferred through the milk of these stressed mothers to their neonates. Despite these increases in corticosterone, the transmammary transfer and accumulation of total and HSV-specific IgG in neonate serum remained intact. This milk-derived, HSV-specific antibody alone protected the neonate from systemic viral spread. Interestingly, postnatal maternal stress significantly increased neonate survival after HSV-2 infection despite no apparent alteration in viral spread. These studies demonstrate that although the transmammary transfer of antibody is unaffected by maternal stress, stress may be enhancing components of antiviral immunity that are effective in protecting neonates from HSV-associated mortality.