Like Zika, infection with Rift Valley fever virus can go unnoticed during pregnancy, all the while doing irreparable – often lethal – harm to the fetus. The results of a new study, led by researchers at the University of Pittsburgh Graduate School of Public Health and the Center for Vaccine Research (CVR), underscore the importance of disease prevention for pregnant women and set the stage for vaccine development.
In a paper published in Science Advances, the researchers show that, in pregnant rats with no outward signs of disease, Rift Valley fever virus is vertically transmitted from mother to child through the placenta, resulting in high rates of stillbirth. Similar results were seen in human tissue.
“I think it’s such a big step forward for the field,” said lead author Dr. Amy Hartman, assistant professor of infectious diseases and microbiology in Pitt Public Health, and member of Pitt’s CVR. “Now we have a way to study in the lab how the virus is transmitted from mother to fetus, with the very important goal of figuring out how to prevent that.”
[Photo: Hartman Lab]
Although Rift Valley fever has been reported only in Africa and the Middle East, the mosquito that transmits the virus also ranges from Europe to the Americas. The World Health Organization (WHO) considers Rift Valley fever a potential public health emergency.
Epidemiology in human pregnancy is scant, but among herds of livestock, Rift Valley fever outbreaks lead to an “abortion storm,” resulting in widespread miscarriage and stillbirth affecting 90 to 100 percent of pregnant animals.
This new study by Dr. Hartman and colleagues establishes for the first time a laboratory-friendly rodent model of the virus’ hallmark gestational consequences.
“Our model is similar to what is seen in livestock,” said first author Dr. Cynthia McMillen, a postdoctoral researcher in Dr. Hartman’s lab. “The adults may have little or no disease symptoms, but still have significant damage to the placenta and their offspring. This observed pathology and vertical transmission of the virus can explain how Rift Valley fever virus infection leads to fetal demise.”
Overall, 65 percent of the pups born of infected rats died, compared to 25 percent of pups born of uninfected controls. All of the infected mothers lost at least one pup, and all of their offspring – living and dead – contracted the virus. The placentas of these animals harbored more virus than any other tissue in the body.
Because the placenta is different among species, it was important to see whether human placenta has the same susceptibility to Rift Valley fever virus infection. So Dr. McMillen and colleagues enlisted the help of Dr. Carolyn Coyne, professor of pediatrics at UPMC Children’s Hospital of Pittsburgh and a leading expert on viral infections of the placenta. Using human placenta tissue, the research team found that Rift Valley fever virus is even better at evading the mother-child barrier than other vertically transmitted viruses, like Zika.
Having these laboratory models in place, the researchers aim to develop vaccines that could prevent Rift Valley fever virus from realizing its potential as a public health emergency.