The neonatal human's immune response to herpes simplex virus infection: a critical review

The neonate has a variety of quantitative defects in its immune response in elements of both the early containment phase and the later curative phase to HSV infection (Table 2). It is likely that the combination of these defects, and possibly others yet to be delineated (IL-2 response, T cell cytotoxicity response, etc.), account for dissemination or for locally progressive illness in newborn infants. It is unlikely that all these defects can be reconstituted by current available modalities (immunoglobulin, interferons, interleukins). One would hope that improving one or a few of these mechanisms may tilt the balance away from dissemination or central nervous system disease and allow the neonate to mature immunologically.