In 2014, an Ebola epidemic tore through West Africa, claiming approximately 11,310 lives. The epidemic received intense international coverage due to its high mortality. Health officials claim a combination of a mobile population, crumbling public health systems, official neglect, and hazardous burial practices contributed to the pervasiveness of the epidemic.
Normally, Ebola circulates among animal hosts like African bats. In fact, scientists suspect a village boy who was infected by a bat in Guinea served as the starting point of the epidemic. This village boy was affected in 2013 and, now in 2016, research has shown a new development in the Ebola story. Two teams of scientists report that a genetic mutation in the Ebola virus has improved the virus’s ability to enter human cells. These studies, which were published in the Cell, suggest the virus may have evolved a new weapon against its human hosts.
Researchers do not understand how the mutation works; however, evidence suggests the mutation helped expand the scope of the epidemic. Patients infected with the mutated version of Ebola are significantly more likely to die as a result.
While the news of a mutated version is startling, it is not unexpected. When reports of the outbreak surfaced, Dr. Pardis C. Sabeti, a computational biologist at Harvard, and her colleges initiated a collaboration with the doctors in Sierra Leone. Ninety-nine different Ebola viruses were isolated from seventy-eight patients and quickly sequenced. Their analysis depicted Ebola quickly moving from patient to patient, gaining new mutations along the way. The worry at the time was the possibility of the mutations somehow speeding up Ebola’s replication. Many of these mutations, however, do not really mean anything. “We know that viruses mutate,” Dr. Sabeti explains. “There was nothing revelatory in that.”
Ebola has seven genes, with each gene encoding a protein. A gene affected by a mutation may end up making precisely the same protein as before or a protein that works exactly the same way.
There was still a lot left to learn about the Ebola genome. After analyzing 1,480 Ebola genomes, Dr. Sabeti and her colleagues were able to trace the virus’s development over the course of the epidemic in an evolutionary tree. The team located a mutation that arose at pivotal point in the outbreak—GPA82V. Viral samples containing this mutation first emerged in Guinea on March 31, 2014. While the original virus shakily spread at low levels in Guinea, Ebola viruses carrying the GPA82V mutation spread explosively across three countries.
GPA82V Ebola carry altered genes that control the mechanism that produces surface proteins. These surface proteins are called glycoproteins and their tips contact human host cells. This contact opens a passageway through which the virus enters.
To understand the effects of the GPA82V, Dr. Luban and his team of researchers created a form of HIV with Ebola’s glycoproteins and observed as this hybrid virus infected human cells. Evidence shows the mutated hybrid virus attacking human cells and other primate cells with a higher success rate compared to the original virus. The mutated form infected four times as many primate cells. However, the mutation did not help the hybrid viruses infect the cells of other species such a cats and dogs.
Studies concerning GPA82V are still ongoing and with a new mutation in the picture, more effort will be poured into understanding the Ebola genome. With such efforts in place, an understanding of the new Ebola mutation may soon come to light.
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