From the Herpesviridae family, the causative infection agents in newborns are HSV-1, HSV-2, VZV and CMV. There are three ways in which the herpes virus can be transmitted: intrauterine, perinatal and postnatal. In newborns, the symptoms are general, non-specific and can affect multiple organ systems, which poses a problem for the infection to be detected and treated in time. All herpesviruses can be latent, i.e., infect host cells for life. During latency, the viral genes are at rest, inaccessible to immune detection, but stimulated by various external factors, they can again go into the active phase and cause a manifest disease. Newborns with HSV-1 infection more often develop a localized form of the disease ("SEM disease"), and HSV-2 infection is more associated with CNS diseases and at the same time, with a worse disease outcome. Congenital varicella syndrome most often occurs in children whose mothers became infected between the 8th and 20th week of pregnancy, and the clinical picture includes: intrauterine growth restriction, scarring skin lesions, ocular disorders, limb and CNS abnormalities, and fetal death and stillbirth. A high risk of fatal neonatal varicella occurs when the mother develops symptoms between five days before and two days after delivery because there is not enough time for the mother's IgG antibodies to develop to protect the fetus. The most common late sequela of congenital CMV infection is hearing loss, often bilateral and progressive. Acyclovir is the drug of choice for neonatal HSV disease, pregnant women with complicated HSV or VZV infection, and individuals with herpes simplex encephalitis, and valganciclovir may improve hearing and neurodevelopmental outcome in symptomatic children with CMV infection.