In less than three years since it struck West Africa in December 2013, the Ebola virus has killed more than 11,300 people in Guinea, Sierra Leone and Liberia.

The hemorrhagic virus spread like wildfire in the region moving with an incredible speed. Health experts primarily attributed this to inadequate healthcare, dangerous burial practices and poverty.

Two new studies published in the journal Cell, however, have identified another reason why the virus spread fast and was very deadly during the 2014 Ebola outbreak: the virus evolved early in the epidemic and the mutation made it more infectious. The mutated Ebola virus is capable of infecting human cells more easily compared with the original version of the virus.

Early on during the epidemic, computational biologists already noticed that the virus was changing. The virus evolving on its own is not surprising though. Health experts say this is what viruses do when they first start to spread.

To know more about the mutation, Jeremy Luban, from the University of Massachusetts Medical School, and colleagues, as well as another team of researchers headed by Jonathan Ball, from the University of Nottingham, conducted experiments with the virus in the laboratory.

One particular mutation stood out. The mutation emerged in the outbreak when there were only about a hundred cases of Ebola in Guinea and spread fast to Sierra Leone, Liberia, Nigeria, Mali and even to the United States.

The mutant form of virus made its way to a Texas emergency room after Thomas Eric Duncan was infected by Ebola in Liberia and was brought for treatment to the United States.

Researchers said that twice as many fatal cases occurred later in the outbreak from the more virulent strain of Ebola compared with the cases involving the earlier strain.

Researchers noted that because the virus was able to infect a huge number of people, it was able to go through mutations that made it more deadly as the outbreak progressed. Earlier outbreaks of Ebola, just like the one that occurred in 2000 and 2001 in Uganda where there were 425 infections, were short and contained, giving the virus little chance to adapt to humans.

The team behind the second study reported that the mutation could be attributed for how far the outbreak has spread.

"Increased infectivity may have enhanced the ability of EBOV to transmit among humans and contributed to the wide geographic distribution of some viral lineages," the researchers wrote.

Researchers of the first study likewise said that the mutation was linked with increased severity of the disease and more deaths during the outbreak.

"GP-A82V was associated with increased mortality, consistent with the hypothesis that the heightened intrinsic infectivity of GP-A82V contributed to disease severity during the EVD epidemic," researchers of the first study reported.

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