Scientists at the National Institutes of Health have developed a mouse model to study the sexual and fetal transmission of Zika virus. This will enable studies to further understanding of how the Zika virus spreads, thereby allowing treatments to be developed.
Zika virus first infected humans in Brazil in 2015. It spread rapidly across south America, and there have now also been smaller Zika outbreaks in mainland America and Asia. The main route through which humans acquire the Zika virus is a bite from an infected Aedes aegypti mosquito.
However, there have also been reports of human-to-human Zika transmission via sexual intercourse and transfer of the virus from mother to fetus. Of particular concern is the fact that babies born to mothers infected with the Zika virus have a 20-fold increased risk of having a brain defect, especially microcephaly.
Data relating to the sexual and uterine transmission of Zika are limited, but it is clear that such transfers are possible. In 2016, sexual transmission of Zika virus was reported in eleven countries (United States of America, Italy, France, Germany, New Zealand, Argentina, Chile, Peru, Portugal, Canada, Spain). The first case of sexual transmission of Zika in 2017 was reported in Florida earlier this week.
The powerful interferon response to Zika infection observed in the mouse has hindered previous attempts to study Zika transmission in mouse models. Scientists at the National Institutes of Health scientists have now developed a mouse line that lacks the ability to produce key cells of the immune system, and so the interferon response is suppressed.
This new Zika mouse model will allow the precise mechanisms by which Zika is transferred from human to human during sexual intercourse or pregnancy to be investigated. Details of exactly when the transfer occurs and by which routes can now be determined. This in turn will allow research into potential treatments to block virus transmission.
Using this mouse model, researchers have already shown that Zika virus was frequently transferred between males and females. Where pregnancies occurred, only some of the fetuses from each female were infected with Zika. Interestingly, among infected fetuses, the Zika virus was detected in a range of fetal tissue types and not just in the brain, where defects have already been observed in humans.
It is hoped that further studies using this new mouse model will help clarify how Zika virus is spread from human to human and how Zika infection impairs fetal development, giving rise to birth defects. Elucidation of the mechanisms will facilitate the development of treatments and vaccines to control or prevent Zika infection.