Effect of pregnancy hormones on herpesvirus and other deoxyribonucleic acid viruses.

Clinical impressions and observations of genital herpesvirus infections indicate that lesions are more persistent and more severe during pregnancy. Several explanations are possible: an altered immune state, increased vascularity and blood flow, and/or increased viral infectivity due to increase in one or more hormones during pregnancy. Studies presented here were directed toward investigating the latter possibility. Herpesvirus, type 2, isolated from a genital lesion was titrated in WI-38 cells in the absence and presence of estriol, progesterone, human chorionic gonadotropin (hCG) and human placental lactogen. Two other deoxyribonucleic acid (DNA) viruses, adenovirus type 7 and vaccinia virus, were included for control purposes. Although estriol significantly inhibited and hCG significantly enhanced the single-cycle production of herpesvirus, there was little or no effect on these hormones on adenovirus. Progesterone, after 48 hours but not after two hours of preincubation, inhibited production of herpesvirus and vaccinia virus but had no effect on aderiovirus. When end-point titers were measured after multiple cycles of viral growth, there were no differences in viral titers with any of the hormones, except for a slight reduction with estriol. Except for the uniform effect of progesterone on DNA viruses, hormonal effects on viral production cannot be generalized from experiments with one virus.