A new study by Chinese researchers indicates the novel coronavirus may have begun human-to-human transmission in late November from a place other than the Huanan seafood market in Wuhan.
The study published on ChinaXiv, a Chinese open repository for scientific researchers, reveals the new coronavirus was introduced to the seafood market from another location, and then spread rapidly from market to market. The findings were the result of analyses of genome-wide data, sources of infection and the route of spread of 93 samples of the novel coronavirus collected from 12 countries across four continents.
The study believes that patient zero transmitted the virus to workers or sellers at the Huanan seafood market. The crowded market facilitated the further transmission of the virus to buyers, which caused a wider spread in early December 2019.
According to the researchers, the new coronavirus experienced two sudden population expansions, including one on January 6, 2020, which was related to the Chinese New Year's Day holiday. An earlier expansion occurred on December 8, implying human-to-human transmission may have started in early December or late November, and then accelerated when it reached the Huanan seafood market.
On January 6, the National Center for Disease Control and Prevention (CDC) issued a second-level emergency response, which the researchers said served as a warning against mass public activity and travel. If the warnings had received wider public attention, the number of cases spreading nationally and globally in mid-to-late January would have been lower, said the researchers.
Patients from Australia, France, Japan and the US - countries with wider samples - have had at least two sources of infection, and the US in particular has reported five sources, the study said. However, based upon limited samples in other countries, the source of most infections is deemed to be the same. In addition to their contact history with Wuhan, some may have been infected in South China's Guangdong Province and Singapore.
Research by team from Nankai University shows new virus has mutated gene similar to those found in HIV and Ebola. Finding may help scientists understand how the infection spreads and where it came from.
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 Sars (severe acute respiratory syndrome) entered the human body by binding with a receptor protein called ACE2 on a cell membrane. And some early studies suggested that the new coronavirus, which shares about 80 per cent 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 to limit the scale of the Sars outbreak of 2002-03, in 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. Many proteins are inactive or dormant when they are produced and have to be “cut” at specific points to activate their various functions.
When looking at the genome sequence of the new coronavirus, 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 [the new coronavirus] 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 and cause a “direct fusion” of the viral and cellular membranes.
Compared to the Sars’ way of entry, this binding method is “100 to 1,000 times” as efficient, according to the study. Just two weeks after its release, the paper is already the most viewed ever on Chinarxiv. 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.
The mutation could not be found in Sars, Mers or Bat-CoVRaTG13, a bat coronavirus that was considered the original source of the new coronavirus with 96 per cent similarity in genes, it said. This could be “the reason why SARS-CoV-2 is more infectious than other coronaviruses”, Li wrote in a paper released on Chinarxiv on Sunday.
Meanwhile, a study by French scientist Etienne Decroly at Aix-Marseille University, which was published in the scientific journal Antiviral Research on February 10, also found a “furin-like cleavage site” that is absent in similar coronaviruses.
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 Centres for Disease Control and Prevention saying there was no evidence off human-to-human transmission. But that assumption was soon invalidated, and as of Wednesday, there had been more than 81,000 confirmed infections around the world.
Chinese researchers said drugs targeting the furin enzyme could have the potential to hinder the virus’ replication in the human body. These include “a series of HIV-1 therapeutic drugs such as Indinavir, Tenofovir Alafenamide, Tenofovir Disoproxil and Dolutegravir and hepatitis C therapeutic drugs including Boceprevir and Telaprevir”, according to Li’s study.
This suggestion is in line with reports by some Chinese doctors who self-administered HIV drugs after testing positive for the new coronavirus, but there is as yet no clinical evidence to support the theory.
There is also hope that the link to the furin enzyme could shed light on the virus’ evolutionary history before it made the jump to humans. The mutation, which Ruan’s team described as an “unexpected insertion”, could come from many possible sources such as a coronavirus found in rats or even a species of avian flu.
(Blogger's Notes: It is a Chinese Communist Party's lie accepted and promoted by WHO that the new coronavirus lie dormant in bats somewhere between 20 and 70 years, then 'crossed over' to humans through unknown species before it emerged at the Wuhan Seafood Market roughly 900 feet from a level-4 bioweapons lab The Wuhan Institute of Virology controlled by the PLA. Logically the Wuhan Virus, I believe, is a genetically-engineered bat-virus artificially inserted with HIV or Ebola genes. Unfortunately it has escaped into the general populace and been infecting and killing people since.)
Related posts at following links:
Wuhan Virus: A Bio-weapon Escaped From The PLA Bio-weapon Lab in Wuhan.