Ebola virus taken from patient blood samples in Mali in November 2014 are helping researchers re-calculate the virus' rate of evolution. | NIAID
A new study suggests that the virus responsible for the ongoing Ebola outbreak in West Africa is not evolving as quickly as earlier reports had suggested, helping to alleviate fears that it could become more contagious and more resistant to current treatments.
"This does not mean that the virus could not become more virulent and that current diagnostics could not fail," said senior author Heinz Feldmann, chief of the laboratory of virology at the National Institute of Allergy and Infectious Diseases, "but it makes it less likely."
He went on to explain that while scientists and others must continue to monitor the Ebola outbreak in West Africa to ensure the virus' rate of evolution holds steady, "we don't have to panic because there is no real evidence that things will dramatically change."
The findings are reported in the 27 March issue of Science.
The Ebola outbreak that started in West Africa in 2013 has been the largest and longest lasting in recorded history. Even so, sequences of the virus have been published just twice, in March of 2014 (using samples from Guinea) and in June of 2014 (using samples from Sierra Leone). Early analyses based on these sequences suggested the virus is mutating twice as fast as observed in previous outbreaks.
Because Ebola diagnostics and some therapeutics like vaccines are based on the specific viral sequence, it is important for researchers to have the most up-to-date virus genome sequence possible.
To further characterize the sequence of the virus in the current outbreak, Feldmann and colleagues analyzed samples a couple months older and further into the outbreak than those analyzed in March and June of 2014. They sequenced samples from patients infected in the West African country of Mali on two separate occasions — in October and November 2014, respectively.
By comparing changes in the genomes of these samples with those in the viruses sampled earlier, Feldmann and his team showed that the samples from Mali hadn't mutated significantly compared to those from earlier in the year. They also hadn't mutated substantially compared to virus samples from earlier outbreaks.
The researchers then used both the March and June sequences and the October and November sequences to re-estimate an average virus mutation rate for the current outbreak. Adding the two new sequences from Mali reduced the average estimate of viral mutation by about two-fold, making it consistent with the rate from past Central African Ebola outbreaks.
Expanding the time frame over which viral samples were evaluated helped the team get a better handle on the evolution of the virus compared to previous analyses, Feldmann suggested.
The researchers' find means that current diagnostic methods, vaccines, and other treatment interventions should remain effective against the virus.
Feldmann and his colleagues are reporting their results at the 7th International Symposium of Filoviruses in Washington, D.C., this week. "We normally run this conference every three years," he said, "but even though we held it last year, we added another conference again this year because of the great interest in and attention to Ebola."