The central hypothesis in this study is that prenatal psychosocial stress induces herpes viral reactivation through type-1 immune suppression and tryptophan degradation through the IDO pathway and decreases serotonin synthesis which possibly accelerates depressive symptoms. It is hypothesized that stress favors reactivation of latent herpes viruses. It is postulated that the IDO pathway and the GTP-CH1 pathway are involved in this relationship. This hypothesis is formulated on the basis of data collected in the parent study (R01-NR005000) which investigated perinatal immune, endocrine and inflammatory changes in pregnancy and the postpartum period as well as reviews of literatures.
The overall purpose of the parent study was to examine the trajectory of postpartum thyroiditis in women identified as at risk during pregnancy compared to those not at risk. Prenatal data and blood samples were collected as part of the study and will be used in this study. The overall objective of this study is to determine if herpes viruses IgG titers are associated with prenatal stress and depression. It is further speculated that herpes viral reactivation is associated with components of the IDO and GTP-CH1 metabolic pathways.