Abstract

Zika virus (ZIKV), a mosquito-borne flavivirus, has been associated with microcephaly and other neurological disorders in infants born to infected mothers. Despite being declared an international emergency by the World Health Organization, comparatively very little is known about the pathogenesis, mechanisms, or behavioral consequences of maternal ZIKV infection in the offspring. Our lab is interested in developing a working animal model to answer some of these questions. Here, we use a rat model of prenatal ZIKV infection to measure the level of infectivity, as well as the rate of viral clearance in both the mother and her pups. We use quantitative PCR to measure the effect of ZIKV on inflammatory gene expression, and examine various aspects of brain development in pups, including cortical thickness, microglia morphology, and apoptosis. Given that pregnancy is also associated with significant immunomodulation, we are also interested in the role that pregnancy has on the impact of ZIKV infection, therefore we compare viral infectivity between both pregnant and non-pregnant female rats. This model will allow us to 1) better understand the mechanisms underlying ZIKV infection and transmission to the fetus, 2) determine the impact of ZIKV infection on the developing fetal brain, and 3) in the future, measure potential behavioral deficits associated with fetal ZIKV infection later in life.

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