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A mutation in the Ebola virus made the epidemic in West Africa even more deadly

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According to two different studies

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Beginning in December 2013, the Ebola virus spread like wildfire across Guinea, Liberia, and Sierra Leone, killing an estimated 11,310 people over the course of three years. The outbreak moved with incredible speed because of a few factors, including lack of adequate health care, poverty, and dangerous burial practices. Now, scientists have identified an additional culprit: a mutation allowed the Ebola virus to better enter human cells and infect people.

The findings are described in two studies publish today in the journal Cell. The first study examined the virus’s genome at different stages of the outbreak and the health outcomes of those it had infected. They found that twice as many people died later in the outbreak from the more virulent strain, compared with people infected with the earlier strain, according to Scientific American. This mortality rate doesn’t necessarily mean that the virus was twice as deadly to an individual: the virus had mutated to be able to infect more people in the same period of time.

The team noted that because the virus infected a huge number of people, it was likely able to mutate and adapt to humans — becoming more deadly as the outbreak progressed. Other outbreaks — like the one in 2000–2001 in Uganda where 425 people were infected — were short and contained, giving the virus little chance to adapt to humans. As the 2013 Ebola virus spread, it mutated, and some of those mutations, the team noted, “proliferated because they conferred an advantage to the virus.”

The second study came to a similar conclusion. It outlined that minor changes in the virus’s DNA can impact how it infects hosts, and that “prolonged human circulation enabled the virus to better adapt to exclusively human transmission.” The study discovered two variations of the virus: one from early in the outbreak, and another that was more widely distributed. When they compared the two, they discovered a mutation that made the virus twice as likely to infect human cells.

The two studies show how complicated epidemics are. In West Africa, the geopolitical and social conditions that made the virus difficult to contain allowed it to spread to an unprecedented number of people. That, in turn, allowed the virus to mutate and become better at infecting humans.

The studies also highlight how rapidly the Ebola virus can adapt in a host population. And that means that prevention and disrupting the chain of infections early on are two of the most important steps in deterring another epidemic.