Fears that the current Ebola epidemic, the deadliest in history, was caused by a more lethal, fast-moving or easily transmissible virus than in previous outbreaks appear to be unfounded, according to a new study.
The study, a genetic analysis published in the journal Science on Thursday, is based on data that indicates the virus has mutated over time in a way that is similar to that of previous, smaller outbreaks.
Researchers say studies of more cases and more recent ones are still needed to confirm these findings. But the new analysis offers encouraging evidence that tests used to diagnose Ebola patients, and vaccines and drugs being developed to prevent and treat the disease, can continue to be based on the typical mutation rate. It also means worries about doomsday scenarios, like the virus becoming transmissible by air seem unlikely, experts say.
“It hasn’t become increasingly lethal or increasingly virulent,” said David Safronetz, an author of the study and a staff scientist for the Laboratory of Virology at the National Institute of Allergy and Infectious Diseases. “The virus — it’s doing what it’s always done.”
Essentially, the study indicates, while this outbreak has infected 24,000 people and killed about 10,000, its scale has to do with where the epidemic erupted — at the intersection of three vulnerable countries — rather than with any unusual characteristics of the virus itself.
The scientists evaluated change in the virus over time by comparing genetic sequencing data from a small number of cases in Mali in October and November with data from patients infected in Guinea in March 2014 and Sierra Leone in June.
They found that the number of mutations was about the same as in viruses in previous outbreaks, suggesting that the virus was not mutating faster. And they reported that the genetic changes they identified were not significant enough to make the virus more transmissible or deadlier.
“It doesn’t suggest that the virus is getting any worse,” said Dr. Thomas Ksiazek, an Ebola expert at the University of Texas Medical Branch at Galveston, who was not involved in the study.
That supports the use and development of virus-specific lab tests and drugs calibrated according to the mutation rate seen in previous outbreaks.
“You would not predict from what they’ve published that we’re going to have trouble with the diagnostics and vaccines and therapeutics” being developed, said Dr. Anthony S. Fauci, director of the National Institute of Allergy and Infectious Diseases, which partly financed the research.
The cases analyzed in the study involved people who became infected in Guinea and traveled to Mali: a 2-year-old girl taken to Mali by relatives in October and an imam who went to Mali in November and whose illness spread to six other people before it was contained. Dr. Heinz Feldmann, chief of NIAID’s Laboratory of Virology and an author of the study, said the team obtained complete genomes from the blood samples of the 2-year-old and three patients in the November cluster.
Data from the March and June blood samples came from two previous studies by other researchers. One of those, using the June samples, reported a mutation rate “roughly twice as high within the 2014 outbreak as between outbreaks,” and said that “because many of the mutations alter protein sequences and other biologically meaningful targets, they should be monitored for impact on diagnostics, vaccines, and therapies critical to outbreak response.”
The authors of that study did not raise alarms about a fast-changing virus, but Dr. Fauci said some misinterpreted it to suggest that there might be problems with lab tests or drugs in development. The Mali study’s results allay those fears, he said.
The study of June samples was larger, with 99 genomes from 78 patients. But since those patients became ill earlier in the outbreak, the later Mali cases make it possible to document change over time.
“We go five months longer into the outbreak and we do not find that this virus has a higher evolution rate,” Dr. Feldmann said. His team used a different algorithm than the June team, and Dr. Feldmann said that when they applied their algorithm to the June samples, the resulting mutation rate was similar to previous outbreaks.
Pardis Sabeti, a Harvard geneticist and an author of the study on the June samples, said the new study was “consistent” with her team’s analysis, which she said found a similar number of mutations. She added, “There is no way to tell if the particular mutations change the biology of the virus without experimental studies. We shouldn’t be alarmist and we shouldn’t be complacent.”
Dr. Feldmann said the next step was to analyze a batch of samples from Liberia from August to the present. The studies to date, including his team’s, “are snapshots,” he said. “The analysis will get much better if we can look at the entire outbreak.”
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