title: Is preeclampsia an infectious disease?
abstract: BACKGROUND
  Studies have suggested a strong paternal factor in the etiology of preeclampsia. If preeclampsia is caused by an infectious agent transmitted by the woman's partner, seronegative women who may experience primary infection in pregnancy should be at increased risk of preeclampsia as compared to previously infected women. The aim of this study was to assess the impact of being seronegative for some viruses transmitted by close contact on the risk of developing preeclampsia.
  
  
  METHODS
  Nine hundred and seventy-eight women were randomly drawn from a basic study population of 35,940 pregnant women in Norway. A serum sample drawn at the first antenatal visit was analyzed for specific IgG antibodies against herpes simplex virus type-2, cytomegalovirus and Epstein-Barr virus. For comparison, antibody status against Toxoplasma gondii was also assessed. Information on preeclampsia in pregnancy was obtained through linkage to the Medical Birth Registry of Norway.
  
  
  RESULTS
  Thirty-three (3%) women developed preeclampsia. The risk of developing preeclampsia seemed to be increased for women who were seronegative for the viruses studied. Seronegativity for Toxoplasma gondii did not show such a pattern.
  
  
  CONCLUSIONS
  Women who are seronegative for antibodies against viral agents transmitted through close contact seem more likely to develop preeclampsia. This finding indicates that women who are seronegative to such agents may acquire primary infection in pregnancy, and subsequently be at increased risk of preeclampsia. This hypothesis could represent a new approach to the causes of preeclampsia, and encourage search for yet unidentified microbes as a possible causal factor.
authors.affiliation: Department of Population Health, National Institute of Public Health, P.O. Box 4404 Nydalen, 0403 Oslo, Norway. lill.trogstad@folkehelsa.no
authors.forename: L I
authors.initials: LI
authors.lastname: Trogstad
authors.forename: A
authors.initials: A
authors.lastname: Eskild
authors.forename: A L
authors.initials: AL
authors.lastname: Bruu
authors.forename: S
authors.initials: S
authors.lastname: Jeansson
authors.forename: P A
authors.initials: PA
authors.lastname: Jenum
mesh_terms: D000293:Adolescent; D000328:Adult; D000818:Animals; D000914:Antibodies, Viral / Q000097:blood; D003587:Cytomegalovirus / Q000302:isolation & purification; D003586:Cytomegalovirus Infections / Q000097:blood / Q000453:epidemiology / Q000821:virology; D020031:Epstein-Barr Virus Infections / Q000097:blood / Q000453:epidemiology / Q000821:virology; D005260:Female; D006558:Herpes Genitalis / Q000097:blood / Q000453:epidemiology / Q000821:virology; D018258:Herpesvirus 2, Human / Q000302:isolation & purification; D004854:Herpesvirus 4, Human / Q000302:isolation & purification; D006801:Humans; D007074:Immunoglobulin G / Q000097:blood; D015999:Multivariate Analysis; D009664:Norway / Q000453:epidemiology; D011225:Pre-Eclampsia / Q000453:epidemiology / Q000276:immunology / Q000821:virology*; D011247:Pregnancy; D011251:Pregnancy Complications, Infectious / Q000097:blood / Q000453:epidemiology / Q000821:virology*; D011446:Prospective Studies; D016036:Seroepidemiologic Studies; D014122:Toxoplasma / Q000302:isolation & purification; D014123:Toxoplasmosis / Q000097:blood / Q000453:epidemiology / Q000469:parasitology
chemical_list: D000914:Antibodies, Viral; D007074:Immunoglobulin G