Neonatal CD8+ T cells are slow to develop into lytic effectors after HSV infection in vivo.

HSV is an important neonatal pathogen. We defined the kinetics of the primary CTL response to HSV-2 in vivo in neonatal mice. Using a replication-defective HSV-2 virus, we demonstrate that neonates mount a primary HSV-specific CTL effector response in the draining LN, with delayed onset and shortened peak activity, in contrast to the rapid, strong response observed in adult mice.

HSV induces an early primary Th1 CD4 T cell response in neonatal mice, but reduced CTL activity at the time of the peak adult response.

Neonates are highly susceptible to HSV. In this study, we analyzed the primary neonatal cell-mediated response to HSV at the site of T cell activation, the draining lymph nodes (LN), and examined the effects of dose and the ability of HSV to replicate on the strength and character of this response. Neonatal mice mounted a predominantly Th1 cytokine (IFN-gamma) response at all doses of a replication-competent thymidine kinase-negative HSV-2 strain (186DeltaKpn) and at high doses of a replication-defective HSV-2 virus (dl5-29, UL5(-)/UL29(-)).

Maternal immunization with a herpes simplex virus type 2 replication-defective virus reduces visceral dissemination but not lethal encephalitis in newborn mice after oral challenge.

Herpes simplex virus (HSV) causes devastating infections in newborns. Maternal immunization is one potential strategy to reduce neonatal HSV disease. Female mice were immunized with an HSV type 2 (HSV-2) replication-defective mutant (HSV-2 dl5-29, which is defective for the genes UL5 and UL29) and then mated.