The liars say it's a "mutation", but in reality it's genetic engineering that spliced the HIV protein into the coronavirus.

Anyway, I told you all that this coronavirus has an HIV protein and it's essentially HIV that spreads like measles or flu, but most of you didn't want to listen. Now, the mainstream sources are coming around to admitting that it's "HIV-like", but they won't admit it's genetically engineered.

Fact is HIV doesn't exchange genetic material with coronavirus in nature. This thing came from a lab.

https://www.scmp.com/news/china/society/article/3052495/coronavirus-far-more-likely-sars-bond-human-cells-scientists-say

Coronavirus far more likely than Sars to bond to human cells due to HIV-like mutation, scientists say

    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
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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.

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.

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