As the senior author of the paper ya'll you are discussing first off I am honored that Caryn and others have commented on our work and findings-this certainly makes a basic scientist feel good that our work may have some real life implications. Secondly, hopefully to clarify, we were able to induce PE-like symptoms in rats by excessively activating the mom's immune system during pregnancy. As Caryn mentioned in somewhat other terms, the mom's immune system is already activated trying to prepare for and accept a half-foreign fetus. This represents a pro-inflammatory state in preparation for these events. What we showed that is that the events associated with pregnancy do not cause PE alone, nor does immune system activation in non-pregnant animals, but the combination of the 2 caused PE like symptoms in animals. Toll-like receptor 3 senses double-stranded RNA (which are rotavirus and rheovirus), but several other factors can activate these receptors during pregnancy. While I would love to prove that every case of PE is caused by previous exposure to rheo/rotavirus, necrotic (dying) cells can also activate TLR3 and other viruses (single stranded RNA viruses such as CMV, HPV, etc. when they divide create double-stranded RNA) can also activate TLR3. We are presently determining whether a mom has to have an active viral infection vs. a latent one as well as whether TLR3 is activated in women with PE vs. normotensive pregnant women. My ultimate goal, if we find that TLR3 is activated in PE women, is to design TLR3 inhibitors as a therapy to prevent PE after it is diagnosed. In support, we have developed a mouse model of the disease, somewhat similar to the rat model in the paper, but we are able to gather a substantial amount more data regarding the possible mechanisms and are now able to test various therapeutics. While it is no consolation to those of you who have experienced PE, hopefully we can treat this in women in the near future.