London, October 29 (The Conversation) Almost three years after SARS-CoV-2 emerged, we still don’t know where the virus that causes COVID-19 came from.
The location of the initial outbreak near the Wuhan Institute of Virology raised suspicions that it was possibly a laboratory leak. But scientists have largely advocated an overflow of herbs from bats to humans, via an intermediate animal host, at the Huanan seafood market. a few kilometers away. To date, however, no immediate ancestor of SARS-CoV-2 has been discovered in bats or any other animal on the market.
A recent preprint (a study that has not yet been peer-reviewed) claims to have known serial patterns in the SARS-CoV-2 genome. These patterns could imply that the virus was genetically modified in a laboratory.
It should be emphasized that any realistic situation of laboratory origin would involve an accidental escape, not a nefarious intention. Viruses have no application as biological weapons in the fashion world. They are difficult to produce in giant quantities and to implement. And if they can spread from human to human, they will most likely spread to unintentional populations, adding friendly forces.
The previous post won poorly through top experts in the field, and many reacted on social media.
This combined reception is largely not surprising. Scientists and members of the general public have strong criticisms about the origin of SARS-CoV-2, despite all the available evidence that remains weak and circumstantial. In the absence of falsified facts, reviews are necessarily based largely on feelings and belonging to the organization, especially when you think there’s a lot at stake.
The genomes of all organisms, in addition to SARS-CoV-2, are made up of long stretches of 4 other nucleotides (A, T, G and C). These are the building blocks of RNA and DNA.
Large viral genomes, such as those of coronaviruses, can be cut into smaller pieces, or fragments, that can be combined and paired to examine the effect of other genes and mutations. Scientists can do this, for example, to perceive which genes or mutations increase the threat of a virus spreading to humans.
The popular approach to cutting viral genomes into smaller pieces is to use restriction enzymes, called molecular scissors. Restriction enzymes recognize and cut express nucleotide sequences (e. g. e. g. , GAATTC) to manipulate viral genomes. These come with type IIS enzymes.
The preprint states that in the SARS-CoV-2 genome, the distribution of certain restriction sites (the places where the genome would possibly have been cut and attached) is “abnormal” and consistent with the virus being sewn from several smaller IIS fragments—type enzymes called BsaI and BsmBI.
In particular, the restriction sites had an excess of silent mutations. These are nucleotide adjustments that do not have the characteristics of the virus and would possibly be characteristics of genetic engineering.
By cutting and assembling IIS enzymes from genomes, scientists can transparently erase all traces of restriction sites through an approach called “golden-gate assembly. “
Therefore, in order for the distribution of IIS-type enzymes in SARS-CoV-2 to be interpreted as an engineering signature, IIS restriction sites have been deliberately left. While it’s not absolutely implausible, it’s not an unusual practice, and scientists have wondered what the explanation would be for why leave those sites behind.
Questions also arose related to some of the mathematical measures on which the authors’ conclusions are based, in particular, the assumed maximum duration of individual viral fragments. Meanwhile, the research was criticized because it thought only the two type IIS restriction enzymes commonly used in this context.
All of these highly technical issues of controversy illustrate the possibility of formulating passable and verifiable hypotheses for complex issues.
What are the odds? The study also explored the ease with which the restriction site distribution trend observed in SARS-CoV-2 can be generated simply through possibility (as opposed to engineering). The researchers simulated a process of random mutations of two close relatives of SARS-CoV-2. The probability of generating the same style low: 0. 1% and 1. 2%.
Once again, this research has been criticized. Coronaviruses can naturally gain and lose restriction patterns through the accumulation of mutations, but also other viral strains exchange genetic material, a procedure called genetic recombination.
Since coronaviruses go through a common genetic recombination, a process of simulating a set of recombination and mutation events would be better suited to answer this question.
This complaint is fair, but partly overlooks the fact that patterns can be informative even if the procedure that generated them is unknown. Only one black sheep stands out in a flock of 1,000, whether the color of its fur is due to a genetic makeup or because it fell into a tar barrel.
The evidence reported in the preprint is neither conclusive nor definitive. These effects may turn out to be a coincidence or generated through a flaw in the method. The authors were largely open about some of the limitations of their paintings and invited commentary and criticism.
While the effects can be replicated across others and remain valid once additional knowledge has been analysed, this study is unlikely to influence many opinions. evidence to the debate.
The reception of the paintings raises difficult questions. For some experts, it is unwise to talk about any evidence to help a lab leak, as it can only fuel conspiracy theories. However, the public belief that existing evidence can be subject to censorship is even more important. It probably has this effect. In particular, China has largely failed to cooperate in investigating the origin of the virus.
The nightmare situation for me would be the eventual confirmation of an accidental laboratory leak, but the confirmation of a laboratory leak whose evidence has been aggressively suppressed. (The conversation) Nsa
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