The new crown is not man-made, and its proprietary features are not available in the laboratory.

The vast majority of the conspiracy theories surrounding the new coronavirus have been falsely identified by the Original Spectrum Duchen silicon star as scientists continue to research it.
however, the source of the virus, whether its original source is a laboratory, is not the human initiative to create a "virus weapon", is currently highly controversial.
foreign people because the outbreak first broke out in Wuhan and blamed the "original explosion point" of the South China seafood market not far from the Wuhan virus, china recently accused the virus from the U. S. military closed last year in a virus laboratory, the U.S. military was brought to Wuhan.
a newsletter published March 17 in the academic journal Nature Medicine, quoting, summarizing and confirming recent research by a team of leading experts.
this article, once again for the virus 'artificial' hypothesis has been strongly refuted.
this article points out that the new coronavirus cannot appear through laboratory-related SARS-type coronaviruses.
authors argue that the hypothesis of "artificial" new crown virus lacks reliable research and is not scientifically feasible at all.
the ability of the new coronavirus's echinoprotein to bind to human cell receptors is lower than any known binding method.
If the new coronavirus is the result of artificial genetic editing, the more effective way is to use known coronavirus B (i.e. human coronavirus) as a blueprint.
, some of the genetic traits unique to the new coronavirus are more likely to occur in zoonotic or human-to-human transmission and cannot occur in petri dishes.
the first author of this newsletter is Kristian Anderson, an associate professor at the Scripps Institution of Comprehensive Medical Research and Educational Institutions.
1, receptor enzyme binding mechanism inefficient coronavirus named after its surface a large number of ratchet protein (S-protein), it looks like a crown.
echidna protein is also home to the binding of the new coronavirus and human cells.
rata protein has two distinct characteristics that are essential in the process of binding to human cells. the first feature of the
is the receptor binding domain (RBD).
in the genome of the new coronavirus, there is a section responsible for the echidna protein, and in this paragraph there is a small section, responsible for the receptor binding domain (RBD).
you can understand that the ratchet protein is the virus to catch the human cell 'touch", and the receptor binding domain, is the "touch" on the "hook." There are six residues (residues) in the
receptor binding domain, which plays a key role in the binding of the echinoprotein and ACE2 receptor enzymes on human cells.
, however, five of the six remnants of the new coronavirus are different from SARS-type coronaviruses, as well as SARS viruses that circulated in Asia in 2003.
researchers found that although the affinity of the new coronavirus and receptor binding was good, it was still not the best.
SARS coronavirus and human cell affinity is better than the new coronavirus, the binding mechanism is better, and this information is known.
in layman's terms, mutations in the neo-coronavirus echinoprotein do not help the virus bind better to human cells.
is a highly likely scenario: the binding mechanism of the new coronavirus and human cells is more likely to be a natural selection than a "man-made" result.
because if someone wants to create a new coronavirus by genetic editing, he can use a known, affinity-friendly combination mechanism, rather than hoping for a variant that is unstable.
2, the author of the article on animal coronaviruses with closer molecular structures, further points out that the second characteristic of the new coronavirus echinoprotein is polybase furin protein cleavage ( and more specifically, the unique effect of this cleavage.
you can interpret this cleavage as a "knife" of the virus: the echidna protein can open a gap after grabbing the body's cells, for injection, fusion, and so on.
without it, the virus is only hanging on the cell, making it difficult to invade effectively.
in the genes of different viruses, the difference in lysate can determine the infection and host range of the virus , say whether the host is a human, an animal, or a zoonotic disease.
researchers found that the polybase of the new coronavirus is a fleodio of Flynn protein, and that it is able to cut the receptor cells using other proteins, such as Flynn.
next, the virus injected a gene that included a proline, a process that computer analysis suggests can form an O-connected sugar base on the cut flanks of cells.
there has been no study to find a specific purpose for this mechanism, but the authors believe it could create an umbrella for key residues that can evade the immune system.
this genetic trait is only present on the new coronavirus and does not appear in other SARS-type coronavirus espressoviruses (B coronavirus spectrum B), which is significantly different from other coronaviruses and is almost non-existent).
the Scripps Institution's website, if anyone wants to create a new coronavirus as a pathogen, he can "develop" the backbone of a known, more pathogenic coronavirus.
But now we see the new coronavirus, whose backbone and known highly pathogenic human coronavirus are not much like, but are closer to those found in bats and pangolins.
3, several possible authors of the new coronavirus origin theory article pointed out that the two genetic characteristics of the new coronavirus, including the variation of the receptor binding domain and the apparent differences in the backbone of the virus, ruled out laboratory manipulation as a potential source of the new coronavirus.
the authors suggest two possibilities that can reasonably explain the origin of the new coronavirus, both of which are the result of natural selection: 1) natural selection in animal hosts before zoonotics occur, and 2) natural selection in human hosts after zoonotic occurs.
first possibility: there have been several studies that have shown that a large number of early confirmed cases are related to the South China seafood market.
with this in mind, there may be animal hosts in the market for the new coronavirus.
Given the 96% similarity in the genetic lineage between the new coronavirus and the bat SARS-like coronavirus (RaTG13), bats may be the storage home of the new coronavirus (non-direct) proviral virus.
, bats may be the earliest and longest-running animal host of the virus in the long process of carrying the virus before it is transmitted to humans.
in the smuggled Malaya pangolin found in Guangdong Province, the Yunnan University team found a coronavirus more similar to the new coronavirus, which was identical on the six key residues of the receptor binding domain.
if the virus from bats and pangolins is a direct proviral virus from the new coronavirus - there is no research to prove it.
However, the authors believe that the most likely animal intermediate host, whose population density should be very high, should allow the virus's mutation (natural selection) to occur efficiently, given the receptor binding domain variation of the new coronavirus and the two genetic characteristics of polybase-to-Flynn protein lysis.
because if the density is not enough, in layman's terms, the virus is likely to mutate itself to death, become lost.
second possibility: it is also possible that an ancestral virus jumps from animals to humans, acquiring the genetic traits of the aforementioned gene in the process of human-to-human adaptation.
on the variation of the receptor binding domain, the authors believe that since this trait has been found on the pangolin-carrying coronavirus, the same the same mutation can be thought to have occurred in humans.
two different studies on polybase-to-Flynn protein cleavage point, from The Silver Lake Hospital and the University of Edinburgh, point to the possibility that, in an earlier period, a new coronavirus without a lysis feature jumped onto a person enough (rather than just skipped once) and then mutated the feature during a limited human transmission.
the same thing happened in the Middle East Respiratory Syndrome. Is it possible for
to escape from the lab? In the study of other SARS-type coronaviruses, receptor binding domain variations were recorded during laboratory cell culture.
, however, the previousmention discovery of almost identical receptor binding domains on coronaviruses in pangolins is more likely to explain that the virus obtains these characteristics in the host rather than in a laboratory dish.
the authors further point out that the new polybase-to-lysis has previously been found only in the long-term spread of low pathogenic avian influenza.
this situation also points to the lack of justification for the cultivation of the new crown virus laboratory.
and, if the new coronavirus is to be cultivated in the laboratory or in animals, it is necessary to have a very complex experimental environment to obtain both the receptor binding domain and the new polybase-to-split.
, for example.
requires an ancestral virus that is extremely similar to the current new coronavirus (higher than other SARS coronaviruses) and must undergo uninterrupted, successful replication culture in a petri dish or animal environment containing ACE2 receptor enzymes (no experiments are known to be available) Most importantly, the new coronavirus produces O-connecting sugar in combination, which is not possible in a petri dish, as it requires the presence of the immune system of living animals.
Source: Original Spectrum Duchen Silicon Star Man.