The new coronavirus has an HIV-like mutation that means its ability to bind with human cells could be up to 1,000 times as strong as the Sars virus, according to new research by scientists in China and Europe.
The discovery could help to explain not only how the infection has spread but also where it came from and how best to fight it.
Scientists showed that the virus that causes Sars (severe acute respiratory syndrome) entered the human body by binding with a receptor protein called ACE2 on a cell membrane.
Some early studies suggested that the new coronavirus, which shares about 80% of the genetic structure of Sars, might follow a similar path.
But the ACE2 protein does not exist in large quantities in healthy people, and this partly helped limit the scale of the Sars outbreak of 2002-03, which infected about 8,000 people around the world.
Other highly contagious viruses, including HIV and Ebola, target an enzyme called furin, which works as a protein activator in the human body.
When looking at the genome sequence of the new coronavirus, also known as 2019-nCoV, Professor Ruan Jishou and his team at Nankai University in Tianjin found a section of mutated genes that did not exist in Sars, but were similar to those found in HIV and Ebola.
"This finding suggests that 2019-nCoV may be significantly different from the Sars coronavirus in the infection pathway," the scientists said in a paper published this month on Chinaxiv.org, a platform used by the Chinese Academy of Sciences to release scientific research papers before they have been peer-reviewed.
"This virus may use the packing mechanisms of other viruses such as HIV."
According to the study, the mutation can generate a structure known as a cleavage site in the new coronavirus' spike protein.
The virus uses the outreaching spike protein to hook on to the host cell, but normally this protein is inactive.
The cleavage site structure's job is to trick the human furin protein, so it will cut and activate the spike protein. The activation causes a "direct fusion" of the viral and cellular membranes.
Compared to the Sars virus's way of entry, this binding method is "100 to 1,000 times" as efficient, according to the study.
In a follow-up study, a research team led by Professor Li Hua from Huazhong University of Science and Technology in Wuhan, Hubei province, confirmed Ruan's findings.
A researcher with the Beijing Institute of Microbiology, Chinese Academy of Sciences in Beijing, said the studies were all based on genetic sequencing.
"Whether (the virus) behaves as predicted will need other evidence including experiments," said the researcher who asked not to be named.
"The answer will tell how the virus makes us ill," he said.
Scientists' understanding of the new coronavirus has changed dramatically over the past few months.
At first, the virus was not considered a major threat, with the Chinese Centers for Disease Control and Prevention saying there was no evidence of human-to-human transmission.
That assumption was soon invalidated. As of Thursday, there have been more than 82,000 confirmed infections around the world.
Chinese researchers said drugs targeting the furin enzyme, including HIV medicines, could have the potential to hinder the virus's replication in the human body,
This suggestion is in line with reports by some Chinese doctors who self-administered HIV drugs after testing positive for the new coronavirus, although there is no clinical evidence to support the theory.
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