The mosquito-borne virus that causes Rift Valley fever may severely injure human fetuses if contracted by mothers during pregnancy, according to new research.
In a study published last month in the journal Science Advances, researchers used infected rats and human fetal tissue to discover how the virus targets the placenta. Results showed that the virus may be even more damaging to fetuses than the Zika virus, which set off a global crisis in 2015 and left thousands of babies in Central America and South America with severe birth defects.
“Zika caught everybody by surprise,” said Amy Hartman, an infectious disease specialist at the University of Pittsburgh, who led the research. “If doctors had known about Zika’s birth effects, they could have done a lot more to protect pregnant women and babies. With Rift Valley fever, we’re trying to get ahead of the curve.”
Rift Valley fever primarily occurs in livestock in sub-Saharan Africa, where outbreaks cause 90 to 100 percent of pregnant cows in a herd to miscarry or deliver stillborn calves, often a significant economic loss.
But hundreds of cases also occur in humans each year, causing flulike symptoms and severe liver problems. The outbreaks have moved beyond Africa: In late 2000, an outbreak in Saudi Arabia infected more than 100,000 people and led to at least 700 deaths, according to Dr. Hartman. The mosquito that carries the disease is also found in Europe and the Americas.
“Climate change can alter how emerging infectious diseases will spread,” Dr. Hartman said. “As mosquito populations move and change, we have a potential for this to spread far beyond its normal boundaries.”
There are no vaccines or treatments for Rift Valley fever. The World Health Organization has called the disease a potential public health emergency.
Two cases of infected fetuses have been documented. One infant was born with an enlarged liver and spleen, among other symptoms; the other died within a week. Because the disease can be asymptomatic in pregnant women, many more cases of abnormalities and stillbirths may have been misidentified.
Among rats used in the study, 65 percent of the pups born to infected mothers died, compared to 25 percent of pups born from uninfected controls. Each infected mother lost at least one pup, and all of the infected mothers’ offspring contracted the virus.
Pregnant rats were also more susceptible to death from Rift Valley fever than nonpregnant rats.
Most surprising to researchers, the infected mothers’ placentas harbored more virus than any other tissue in the body — more than even the liver, where the virus’s damage is typically observed.
“No one in the field recognized this before,” said Cynthia McMillen, a postdoctoral researcher in Dr. Hartman’s lab, and one of the study’s lead authors.
Testing on human placental tissue revealed that, unlike the Zika virus, Rift Valley fever virus has a unique ability to infect a specialized layer of cells that supports the region of the placenta where nutrients flow in.
Zika must take the “side roads” into the placenta to infect a fetus, while the Rift Valley fever virus can take the “expressway,” Dr. Hartman said.
“The fetus is protected from hundreds of thousands of dangers that could affect it,” she added. “Only a few microbes can get past, and this is one of them.”
Last week, the Coalition for Epidemic Preparedness Innovations launched a call for proposals to develop human vaccines against Rift Valley fever. About $48 million will finance up to eight projects on Rift Valley fever and Chikungunya viruses, according to an announcement.
“We need more research into the epidemiology — how it causes disease, and how to prevent it,” Dr. McMillen said. “This could spread beyond where it is found in the Middle East, so awareness is sorely needed.”
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