Two teams of scientists independently discovered that even at the beginning of the current Ebola epidemic, the virus mutated and began to infect human cells better.
The sharp outbreak of the Ebola epidemic, which began in 2013 and swept the countries of West Africa, has not yet ended, but has already puzzled specialists. Previously, the disease did not affect more than a few hundred people, but this time there were tens of thousands of them. The virus has reached large cities and, judging by the latest data, has rapidly mutated. Two articles published by Cell magazine tell about this at once.
The first publication was written by teams of biologists at Harvard, led by Pardis Sabeti, and by Jeremy Luban's team at the University of Massachusetts. They analyzed the genomes of Ebola viruses isolated from 1,489 African patients during the 2013-2016 epidemic. It found that by March 2014, when the problem began to take hold (and about three months after the first case was reported), two separate strains could be detected.
In one of them, one amino acid was replaced in the viral envelope glycoprotein - in the region that is required for its interaction with the host cell membrane. Soon, the mutant completely replaced the competing strain. The authors did not get access to work with a dangerous virus, so they were unable to conduct direct experiments in order to find out whether the mutant strain is more virulent. However, they did indirect experiments by constructing artificial analogs of real viruses carrying the corresponding genes of both strains. The mutant form of this model infected the cell culture much more efficiently than the original one.
Approximately the same conclusions were reached by European researchers, the authors of the second article - Jonathan Ball from the University of Nottingham, Etienne Simon-Loriere from the Pasteur Institute and their colleagues. They used their own set of blood samples from 1,610 people with fever, also finding a mutation in the corresponding glycoprotein. Independently of the US scientists, they also experimented with model viruses, but the team used different cell cultures.
In particular, they found that, having mutated, the virus became worse in infecting the cells of its previous key host, the Hypsignathus monstrosus bat, but better in humans. The authors found a number of other mutations that can increase the virulence of the new strain in relation to humans.
At the same time, both scientists are extremely cautious about the fact that it was mutations and the emergence of a new strain that caused an unusual outbreak of the disease in Africa in 2013-2016. Perhaps the key role was played by the first recorded release of a rare and dangerous fever in large metropolitan areas, where the spread of the virus is much faster, and it is much more difficult to limit it.
Sergey Vasiliev
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