Researchers from Boston University have discovered a common pattern of immune response in monkeys infected with the Ebola virus, which presents itself four days before the arrival of the first symptom, which is usually fever.
As reported in the journal Science Translational Medicine, this suggest a potential biomarker that could be used to diagnose the disease earlier than previously possible, reducing the mortality risk from the virus. Currently, Ebola can only be diagnosed once the symptoms have appeared, such as fever, headaches, and muscle pain. These symptoms can manifest around two to 21 days after being infected.
“If you can start treating someone very, very early on after exposure, they’re less likely to develop really severe disease,” co-first author Dr Emily Speranza said in a statement. “And if you can identify people who are sick before they even show symptoms, you can better quarantine and actually control outbreaks.”
“Right now, we wait for diagnosis until the virus spills out of primary infection sites into the blood. At that point, it’s already tremendously far along.”
The monkey model received the infection through the mucosal surface of their nose, similar to how humans may be infected. Twelve monkeys were studied, some died by day 10, some on day 13, another group by day 21-22, and two animals didn’t get sick at all.
“Prior to this result, there was no model that behaved like the disease that you and I would get, which is, we would probably be exposed, we’d walk around for somewhere between 2 and 21 days, and then we’d get sick,” added John Connor, who is senior author on the paper. “And that’s what this was trying to model: If I get sick in 5 days, and you get sick in 12 days or 17 days, are our immune responses different? All of a sudden you can ask that question.”
The team looked at immune responses from the animal and discovered that no matter how long it took the animal to develop the fever, four days before the spike a handful of genes would be triggered by signaling proteins known as interferons. The team compared their findings in the animal models to blood samples of victims of the 2014-2016 Ebola outbreak in Guinea.
“We found not only the same genes going up,” she says, “but in a similar order.”
The team is now looking into how to use this new information and build it into a biomarker for the infection.