A study by scientists at Rocky Mountain Laboratories has quieted concerns the Ebola virus had become even deadlier to humans due to a mutation during an outbreak that claimed more than 10,000 lives in western Africa.
Last week's release of the National Institutes of Health study coincided with news of a new Ebola virus outbreak in the Democratic Republic of Congo that reportedly has killed 18.
The Ebola virus causes a serious illness that is often fatal if not treated. The virus is transmitted to people from wild animals and then spreads through the human population when people come in contact with bodily fluids like saliva, vomit or urine.
First identified in 1976, the Ebola virus’s impact was limited to a few thousand people in central Africa before the disease swept through Liberia, Guinea and Sierra Leone between 2013 to 2016 in an outbreak that sickened more than 30,000 people and eventually killed more than 10,000.
Early on during that epidemic, scientists speculated the genetic diversity in the circulating Mokona strain of the virus would result in more severe disease and higher rates of transmissibility between humans than prior strains.
RML staff scientist Andrea Marzi was one of 16 National Institutes of Health researchers who traveled to Africa during the outbreak to help facilitate the treatment of people affected by the disease.
Marzi worked with NIAID’s Laboratory of Virology chief Dr. Heinz Feldmann in a subsequent study to determine if mutations during the epidemic had made the disease more deadly to humans.
“At the end of 2016, there were some publications coming out hypothesizing that the Ebola virus Makona — which was the causative agent of the epidemic that devastated West Africa from 2013 to 2016 — might have over time adapted to humans and therefore spread so widely and caused this big epidemic,” Marzi said.
Since RML researchers were involved early on in the response to the outbreak, they had samples of the virus from the beginning in Guinea. They also had samples from Liberia and Mali that included the mutations that were associated with human adaptation of the virus.
The researchers in Hamilton wanted to test the theory that mutation made the disease more deadly to humans by using animal models that were often used in this type of research.
Specially bred mice that are very susceptible to all types of diseases and rhesus macaque monkeys were infected with the various virus isolates to both assess the disease progression and see how the virus would shed.
“We were unable to find any significant differences between early and late isolates lacking or carrying those mutations, suggesting that these mutations did not lead to alterations in the disease-causing ability in animal models,” the researchers’ study said.
While the test subjects weren’t human, they were as close as researchers can come in analyzing these types of research questions, Marzi said.
“Having said that, we were very surprised to see basically no difference,” she said. “The mutation does not seem to contribute to more severe disease of pathogenesis.
“Even though the virus might have adapted to humans by acquiring this mutation … it did not make the disease worse in humans,” Marzi said. “Also we do not think it made it spread more. The study did not show the virus is more easily transmitted via saliva, urine or feces or so (on). We didn’t see a difference between early isolates and later ones carrying the mutation.”
The take away message was that different reasons, other than changes in the virus, likely caused the outbreak to be so widespread and severe.
“Other factors, including socio-economic ones, may have contributed,” Marzi said. “Unlike other outbreaks that occurred in central Africa in small villages where there wasn’t a lot of traffic, western Africa is highly populated and people travel a lot between countries. There is a lot of trade.
“The cities that were infected were not small villages,” she said. “They were like the capitals of those countries with a million people living there. Once the virus gets there, it spreads faster. This may have contributed, too, not just that the virus mutated and adapted to humans. … Our data doesn’t support that hypothesis. Mutations in viruses are normal. It may have moved wider because there were a lot more targets.”
People in West Africa were also slow to react because the disease had not appeared there before.
“In central Africa, people are very aware that Ebola is around,” Marzi said. “If someone presents with symptoms, village elders isolate them. (They) know that it could spread and be devastating. In West Africa in the beginning, nobody believed Ebola was there. They had to raise awareness that something bad was going on.”
Marzi spent two months working in Africa during the outbreak in what she calls an opportunity of a lifetime.
“For me, as a researcher, for the first time I personally could contribute something on the ground level,” she said. “Even though my skills as a scientist are so abstract to many people, those skills actually helped people directly.
“I could determine which people were really sick from blood that was drawn,” Marzi said. “Health care workers could limit the contact from the people who were infected to those people who were not infected and hopefully ensure they didn’t get the virus.”
There was some fear that went along with going into a place where so many were sick and dying.
“I washed my hands in bleach so many times that I could smell it for months afterwards,” she said. “It was quite something, but it was also one of the best things that I did in my life.”