In 2015, the world was shaken by the news of an emerging pathogen called Zika virus. At the time of it’s announcement, this mosquito borne virus was connected to the increase of microencephaly in South America newborns. Newborns with microencephaly have characteristically small heads and are at significant risk for developmental delay. While Zika virus was associated with increased microencephaly rates, it was unknown if the virus itself was causing the observed birth defects. Thus, there was a big push to figure out exactly what the risks of Zika virus infection were, and how to control the virus.
Because Zika virus was rarely associated with human disease prior to the 2015 outbreak, it received little attention from researchers and research funding agencies. This meant that scientists had to rapidly establish experimental methods to study Zika virus, either by creating new methods or adapting old methods. For instance, new mouse models were developed allowing scientists to begin to tease apart the complexities of Zika infection in mammals.
Szaba et al. are one group studying maternal Zika infection using a mouse model. They began their study by infecting adult female mice with Zika virus. The infected mice showed very few signs of disease, similar to Zika virus infection in healthy human adults. The mice were then impregnated, and the health of the fetus was monitored. Despite the lack of symptoms in the mother, the placenta was severely damaged, impeding blood flow to the fetus. While direct infection of the fetus was not observed, the damage to the placenta during infection was enough to cause developmental delays in the fetus.
The mouse model developed by this group mimics human infection. However, findings from this model must be interpreted with caution because mouse physiology and immunity differ from humans in many respects. Nevertheless, this mouse model can be useful for pre-clinical testing of Zika antivirals and vaccines, as well as undoubtedly help us better understand how Zika virus infection causes microcephaly in newborns. Beyond Zika, these studies may also help us understand new aspects of maternal physiology and how other congenital infections cause disease.
Summary written by: Mackenzie Thornbury
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Zika virus infection in immunocompetent pregnant mice causes fetal damage and placental pathology in the absence of fetal infection
Frank M. Szaba, Michael Tighe, Lawrence W. Kummer, Kathleen G. Lanzer, Jerrold M. Ward, Paula Lanthier, In-Jeong Kim, Atsuo Kuki, Marcia A. Blackman, Stephen J. Thomas, Jr-Shiuan Lin