130 dead.
500 infected.
And likely more on the way.
Global health officials are staring down a new outbreak. Not the usual Ebola strain. This one is caused by Bundibugyo a rare species of orthoebolvirus that doesn’t play by the same rules as its cousins.
The WHO declared a public health emergency of international concern back in May. That is their highest alarm.
It shouldn’t come as a shock that the response has been complicated.
What are we dealing with
Think of the Ebola family. It belongs to a group called filoviruses.
There are four main players in the human disease club: the Sudan virus the Taï Forest virus the Bundibugyo virus and then there’s the main event the Ebola virus formerly known as the Zaire virus.
The Zaire strain caused the biggest horrors we’ve seen. Bundibugyo?
It’s a ghost compared to that.
Until now we’ve only seen two other outbreaks of Bundibugyo. One in Uganda in 2005 when scientists first caught a glimpse of it and another in the Congo in 2015. Rare stuff.
Symptoms don’t care about the name though.
Early on you get hit with a fever. Headache. Body aches that feel like you were run over by a truck. Fatigue.
Then it gets darker. Vomiting. Diarrhea.
These aren’t just inconveniences. They lead to dehydration. Death.
The virus also triggers a massive inflammatory response. It infects immune cells and turns them into weapons that destroy the host from the inside. Bleeding. Organ failure.
Is it worse than the “regular” Ebola?
Not quite.
Un-treated Zaire Ebola has a fatality rate up to 90%. Even with treatment that can be 60%.
Bundibugyo hovers between 30% and 50%.
Elke Mühlberger a professor at Boston University calls the idea that this is “mild” cynical.
She’s right. One in three people dying isn’t a soft landing. It’s a graveyard.
But here is the kicker. The immune system fights differently here.
Steven Bradfute an immunologist at the UNM Health Sciences Center points out that the classic Ebola virus is incredibly good at blocking your innate immune system. That’s the first line of defense. The alarm bell.
Bundibugyo isn’t as good at silencing that alarm.
Because the alarm rings the body fights back a little better. The virus is slightly less effective at masking its presence.
No easy buttons
So we have a problem.
We don’t have the right tools for the job.
Currently there is nothing specific for Bundibugyo. No vaccine. No antibody treatment.
Just supportive care.
Why?
The genetic differences matter. When scientists sequenced Bundibugyo in 200 it turned out to be more than 30% different from the other viruses in the family. That might not sound like much. But in virology 30% is an ocean.
Erica Ollmann Saphire at the La Jolla Institute for Immunology breaks it down.
The existing antibodies for Zaire Ebola? Useless here.
“Bundibugyo is different enough that the vaccine for Ebola may not induce sufficient cross- reactive protection.”
We need cross-reactivity. We need one shot to stop multiple viruses.
Right now we have early candidates that work in animals.
Does the industry care?
Not really.
Profit isn’t the driver for a virus that affects remote pockets of Central Africa.
The big drug companies aren’t rushing to finish clinical trials.
“You never know what the next virus is.”
Mühlberger is tired of saying it. Everyone knows we need broad-spectrum antivirals. Broad vaccines.
The science exists in test tubes and mouse models.
The money does not exist in the ledger.
So we track. We treat with water and salts. We pray the alarm bells ring loud enough this time.
What happens when the next outbreak starts in a place where the labs aren’t close by?
We’ll find out soon enough.
