> The presence in SARS-CoV-2 of a 19-nucleotide RNA sequence encoding an FCS at amino acid 681 of its spike protein with 100% identity to the reverse complement of a proprietary MSH3 mRNA sequence is highly unusual. Potential explanations for this correlation should be further investigated.
SARS-CoV-2 injects people with rna that induces viral fragment production in human cells. It was always a tradeoff between a small non-reproducing set of viral proteins, a full-blown self-reproducing infection of the entire virus that spreads to others, or an endless series of lockdowns (there apparently isn't a possible world where all the countries coordinate to exterminate covid directly).
The next question, to my mind, is "How common is that cleavage site in other viruses, especially other viruses endemic to the origin location of SARS-Cov-2?" With a follow-up of "How possible would it be for multi-virus splicing to generate that sequence from two otherwise-unrelated, possibly damaged sequences ending up head-to-tail in the DNA of a host cell?"
We know of other novel viruses that have resulted from sequences of multiple viruses being spliced together in a living host naturally. I don't know how we'd disambiguate that possibility from human synthesis.
Most of them are irrelevant noise but some likely alter behaviour.
The influenza virus is more inviting to evolution due to having multiple nucleoproteins. If multiple strains of influenza manage to infect the same cell, the virions produced will contain a mixture of the nucleoproteins. The process is called reassortment.
Corona on the other hand has only one conneted RNA strand.
This is only what I gathered from the internet, not an expert on this.
"The SARS-CoV-2 virus has some key differences in specific genes relative to previously identified coronaviruses — the ones a laboratory would be working with," said Adam Lauring, an associate professor at the University of Michigan Medical School and an expert in the evolution of viruses.
What about the SARS-CoV-2 virus being a chimera of 2 other viruses? Is that wrong, or not unusual, or irrelevant? Sorry if I’m barking up a wrong tree...
Modern molecular techniques don't really have to leave signs. Indeed scientists synthesised a copy of sars-cov-2 from the sequence data a few months after the sequence was published:
"it is possible for researchers to reconstruct the virus in a lab, using either fragments of virus from patients, or fragments of DNA that are synthesised chemically by biotech companies. " https://www.varsity.co.uk/science/19172
It seems you can basically type any sequence you want and have it made up.
"Furthermore, if genetic manipulation had been performed, one of the several reverse-genetic systems available for betacoronaviruses would probably have been used19. However, the genetic data irrefutably show that SARS-CoV-2 is not derived from any previously used virus backbone"
the SARS-CoV-2 genome is ~29.8K nucleotides long. 96% of that sequence is identical to the genome of RaTG13, i.e. all but ~1200 match. for reference, SARS-CoV-1 is only 82% similar to SARS-CoV-2. at a mutation rate of 8*10^-4, this means the current strains of COVID are ~97% identical to the original 2019 sequence.
so, darned close honestly. to be clear, I'm not saying RaTG13 is the source of the lab leak - it's just too different - but I am saying that it's much closer than the original SARS, and thus had no business being analyzed in a BSL-2 lab.
Does your single-issue account mean to suggest that sequencing a close-ish relative of COVID in 2018 means they were growing it in a lab? I can‘t think of a good explanation that would link sequencing to lab experiments.
RATG13 is 96% similar to Sars-cov-2 which means there is a staggering 1200 mutations between them. For reference, Delta and Omicron are both about 40-70 mutations away from OG Sars-COV-2. And that‘s after 2 very good years for Sars-COV-2 evolution!
Can something like this be done to compare/translate subsequences COVID genetic code to SARS and other virus genetic codes. Would be interesting how much overlap there is. And would further the research into where it came from.
I am not a molecular biologist or virologist, far from it. I am reading the manner in which people who are those things are responding. Some quite scientifically, and others dogmatically. The one tidbit of information I had heard about the FCS was that the SARS-COV-2 had the exact 12-nucleotide sequence, no more no less, so it was an exact match for an FCS proposed for study that was rejected by the DoD, DARPA, or some other U.S. government agency. I believe this is not the same in the other SARS-COV viruses, at least not exactly 12, but found somewhere along a sequence. Can someone here clarify this for me as a layman? I'd appreciate it. It is fascinating to me, and as a result I just picked up an Introduction to Genomics book by Arthur Lesk. Thank you.
I was under the mistaken belief that SARS-CoV-2 lacked RNA Pol proof-reading, so that is my bad there and responsible for my equivocation between it and HIV.
I completely accept that not only is it likely that there will be the viruses sharing the same cytoplasms on occasion, in large enough numbers, on long enough infections, etc etc - because one thing we know about biology is how slippery and stochastic things become, but the fact they dont generally share the same host does make this more of an interesting edge case I would imagine.
Thanks for your interesting links and thoughtful reply!
Not really, no. They specifically pick genomic sequences believed to be unique to SARS-CoV-2; they're specific enough to distinguish between SARS-CoV-2 and the other known coronaviruses, let alone less related viruses.
reply