Purpose of review: Neonatal infection by herpes simplex virus (HSV) 1 or 2 presents a devastating burden to new parents, due to the unpredictability of severe clinical outcomes, as well as the potential for lifelong reactivation. While just under half of neonatal HSV infections have mild clinical impacts akin to those observed in adults, the other half experience viral spread throughout the body (disseminated infection) and/or the brain (central nervous system infection).
Summary: Here we summarize current data on clinical diagnostic measures, antiviral therapy, and known factors of human host biology that contribute to the distinct neonatal outcomes of HSV infection.
Recent findings: We then explore recent new data on how viral genetic diversity between infections may impact clinical outcomes. Further research will be critical to build upon these early findings and to provide statistical power to our ability to discern and/or predict the potential clinical path of a given neonatal infection.
Keywords: Neonatal; comparative genomics; encephalitis; herpes simplex virus; human herpesvirus 1; human herpesvirus 2.