On a molecular basis, HPV 16 has
been shown to both transfect extravillous
trophoblast cells and undergo a complete
lifecycle.6,7 From 3 to 15 days posttransfection,
infected cells demonstrate
decreased viability, 5-fold higher rates of
apoptosis, and progressively and signifi-
cantly decreased invasiveness into an extracellular
matrix.6 This was thought to
be attributed to decrease in E-cadherin
expression, which is an essential cell-cell
adhesion molecule.18 Similarly, HPV 31
infection of trophoblasts lead to decrease
in cell number and endometrial cell
adhesion.11 At the placental level, and
after HPV infection, trophoblasts fail to
remodel and the spiral arteries remain
similar to the nonpregnant state, ie, more
tortuous, thick walled, and narrow, and
therefore may increase the risk of
thrombosis and preeclampsia.9 A failure
to establish normal placentation may
lead to spontaneous abortion in the most
extreme cases, but if the pregnancy does
continue, the abnormalities established
early on may contribute to the development
of preeclampsia. Although the association
between HPV infection and