How does the Ebola virus mutate and infect humans? (Above)

In December 2013, in a small village in Guinea, the Ebola virus left its traditional host bat and infected a young boy.
spread across species led to the largest Ebola outbreak in human history.
, the virus was as prevalent in Guinea alone, with only a few hundred people infected.
the warm weather caused the virus to "catastrophically boil" in the spring of 2014.
cases have soared as the Ebola virus has spread to Sierra Leone, Liberia and other countries.
2016, more than 28,000 people had been infected, 11,000 of whom died.
ebola outbreak has given the virus ample opportunity to adapt to its new host, humans.
early 2014, two independent teams of scientists discovered an Ebola virus variant called A82V.
variant infects bat cells is weak, but it is more suitable for infecting humans.
once a mutated virus appears, they quickly trigger a new outbreak.
the mutant virus has spread outside Guinea and is responsible for most cases of infection.
but both teams stressed that the mutation does not cause the virus to spread exponentially.
team led by Jonathan Ball, a virologist at the University of Nottingham in the UK, found that while the A82V was linked to a large outbreak of the Ebola virus, other factors could be more important, such as the entry of infected people into urban areas and the lack of appropriate funeral measures.
scientists don't find a mutant virus, it could lead to even greater disaster.
it is clear that the virus has begun to adapt to the human body.
, a member of the Broad Institute team, said: 'The mutation occurred a few months after the Ebola outbreak, and if we had stopped the virus earlier, it probably wouldn't have happened.'
reminds us of the importance of getting involved in an outbreak as soon as possible and not to give these viruses the opportunity to adapt and reproduce in humans.
until recently, many researchers doubted whether the Ebola virus had really adapted to humans, said Jeremy Luban, leader of the research team at the Broad Institute in New York.
say there is no hard evidence that any other virus has killed so many people than Ebola.
To refute this claim, scientists compared the genomes of 1,500 viruses since the outbreak of Ebola and found that they belonged to two major genealogies, the first causing the outbreak in Guinea and spreading it within its territory, and the second replacing the first and beginning to spread outside Guinea.
the latter apparently evolved from the former and is very different from previous mutants.
, the A82V variant appears to be particularly important because it affects small molecules on the surface of the virus called glyproteins.
if you look at the Ebola virus under a microscope, you'll see long knotted tubes covered with tiny nails, which are glycoproteins.
they are incorporated into the host cells like keys to the lock, opening the door to infection.
A82V variant appears to have changed the shape of the virus key.
to figure out how these mutations affect viruses, scientists isolated glycoproteins and fused them into the shells of other viruses.
show that the fake virus, which looks like Ebola, cannot replicate or spread.
when these fake viruses pass through the glycoproteins of mutants, they are two to four times more likely to infect human cells than standard viruses.
coincidence, Bauer's team has been conducting similar experiments.
they studied a wider range of mutations and used their own fake viruses.
they came to the same conclusion: A82V enhances the Ebola virus's ability to penetrate human cells.
not just humans, Luban's team found that mutant viruses could better penetrate the cells of chimpanzees and monkeys, but did little for cats, dogs and mice.
and Bauer's team found that the ability of these mutant viruses to infect common host bat cells declined.
the Ebola outbreak, the virus seems to be evolving, from being good at infecting bats to being more susceptible to humans.
when the two teams came to the same conclusion, the importance of their findings was self-evident, and mutant viruses were indeed more adaptable to human cells.
source: Scienceman NetEase Technology reports.