Reproductive Toxicology 21 (2006) 421–435 Review Parvovirus B19 in pregnancy Zivanit Ergaz a, b , Asher Ornoy a, ∗ a Laboratory of Teratology, Department of Anatomy and Cell Biology, Hebrew University Hadassah Medical School, Jerusalem, Israel b Department of Neonatology, Hadassah University Hospital Mount Scopus, Israel Received 18 August 2004; received in revised form 7 January 2005; accepted 14 January 2005 Available online 16 February 2005 Abstract Parvovirus B19 is a widespread infection that may affects 1–5% of pregnant women, mainly with normal pregnancy outcome. The prevalence of infection is higher during epidemics – between 3 and 20% with sero-conversion rate of 3–34%. Infection during pregnancy can cause a variety of other signs of fetal damage. The risk of adverse fetal outcome is increased if maternal infection occurs during the first two trimesters of pregnancy but may also happen during the third trimester. It is a significant cause of fetal loss throughout pregnancy, but has a higher impact in the second half of pregnancy when spontaneous fetal loss from other causes is relatively rare. Parvovirus infection can cause severe fetal anemia as a result of fetal erythroid progenitor cells infection with shortened half life of erythrocytes, causing high output cardiac failure and therefore nonimmune hydrops fetalis (NIHF). The P antigen expressed on fetal cardiac myocytes enables the Parvovirus B19 to infect myocardial cells and produce myocarditis that aggravates the cardiac failure. Although there are several reports of major congenital anomalies among offspring of mothers infected by Parvovirus, the virus does not seem to be a significant teratogen. Since Parvovirus B19 infection can cause severe morbidity and mortality, it should be part of the routine work up of complicated pregnancies. Risk assessment for maternal infection during pregnancy is especially important during epidemics when sero-conversion rates are high. © 2005 Elsevier Inc. All rights reserved. Keywords: Parvovirus B19; Pregnancy; Nonimmune fetal hydrops; Anemia Contents 1. Introduction ........................................................................................................ 422 2. Parvovirus B19 ..................................................................................................... 423 2.1. Taxonomy .................................................................................................... 423 2.2. Morphology .................................................................................................. 423 2.3. Genetics ..................................................................................................... 423 2.4. Proteins ...................................................................................................... 423 2.5. Viral life cycle ................................................................................................ 424 2.6. Culture ...................................................................................................... 424 ∗ Corresponding author. E-mail addresses: ornoya@zahav.net.il, ornoy@cc.huji.ac.il (A. Ornoy). 0890-6238/$ – see front matter © 2005 Elsevier Inc. All rights reserved. doi:10.1016/j.reprotox.2005.01.006