Table 1.

Factors influencing fetal HSV or CMV infection

	HSV	CMV
Mechanical barriers	Generally an ascending infection [42, 43] Transit may be limited by anatomic barriers (cervical plug; fetal membranes) and antimicrobial peptides [41]	Generally a transplacental infection [55]
Site of latency	Resides in neurons (dorsal root ganglia); may not have access to uterine structures after reactivation	May reactivate from white blood cells in uterine tissue [45]
Effect of maternal antibody	More relevant to neonatal disease (discussed below)	Neonatal Fc receptor may facilitate transplacental transmission, especially in presence of low-avidity maternal antibody [63]
Presence of viral receptors	Not known to influence HSV infection of fetus	Spatial regulation of putative CMV receptors may influence infection [69]
Viral factors	Latency is limited to neurons, which may influence likelihood of transplacental spread	Infection may influence placental cell structure and function [64].