Godstud wrote:Comparing a disease to a car? That even dumber than when people compare guns to cars.
Youtube videos are your conspiracy source material. Of course they are!!!
Hmm. The first video mentioned that gain of function research was halted in the US in 2014 for ethical reasons, but resumed in 2017. So stopped under Obama and started again under Trump. I thought you didn’t like Trump. Why didn’t you jump on that as a reason to caste blame for this pandemic? Too dumb?
I noticed you didn’t answer the question of whether you had studied genetics or evolution. So the answer is no? Which would explain your inability to construct a counter argument.
The alternative hypotheses is it evolved in the wet market environment. We already know holding stressed wild animals in close proximity is an ideal environment for cross species viruses to evolve. I previously suggested on another thread that two viruses simultaneously infected a cell could produce a chimera virus.
From a study some years ago on the SARS 1 virus.
https://jvi.asm.org/content/84/7/3134#sec-1Thus, clear evidence for SARS-CoV tracking along ACE2 receptor orthologs was established by these studies, especially between civet and human hosts. However, the receptor for Bat-SCoV in bats remains unclear. It is possible that the immediate progenitor for the SARS-CoV epidemic strain has not been identified; alternatively, recombination insertion of variant RBDs may have mediated the initial cross-species transmission event from bats into other mammals.
The article previously explains how the region’s of the spike protein could be modular, thus facilitating rapid adaption of entry to host cells.
The article is also of interest as it warns of future covid epidemics.
The next article puts it is simpler terms.
https://theconversation.com/coronavirus-origins-genome-analysis-suggests-two-viruses-may-have-combined-134059So it is certainly possible for the binding site region to change rapidly.
https://www.nature.com/articles/s41591-020-0820-9The region marked ‘a’ is the binding region that has changed to match the ACE2 receptor site. Low similarity between the SARS-2 and RaTG13 virus in the region (overall they are quite similar, but not at this binding region) doesn’t mean much as we know from the earlier article that region can change dramatically. This also means a pangolin stage is not absolutely necessary for the evolution of SARS-2.
It is the region labelled ‘b’ that is in question. SARS-2 has a complete section which codes for the cleavage site (this allows the virus membrane to merge with cell membranes by being cut table by human enzymes).
Could it be the result of recombination between viruses in hosts at a wet market or was it done in a lab?If you think it was not done in a lab, you need to explain how it could occur naturally. Simplify crying conspiracy theory because you don’t understand the issue is not good enough.