There's not gain of function. The WIV1 virus already binds to hACE2, putting another spike on it and finding that spike also binds to hACE2 in vitro doesn't enhance its function at all. It does tell you how much that spike binds to hACE2.
You can debate if that's a good idea or not, but SARS-CoV-2 is way too distant from WIV1/SARS-CoV-1 to arise from any lab experiment with chimeric viruses. And its also too far away from RaTG13, which still needs decades of evolution to turn into SARS-CoV-2.
> The work met--unequivocally--the definition of gain-of-function research of concern under the 2014 Pause.
> The work met--unequivocally--the definition of potential pandemic pathogen enhancement under the 2017 HHS Potential Pandemic Pathogen Control and Oversight (P3CO) Framework.
2) You only read the title of the article I linked that was in sub-tweets. See the following tweet:
https://mobile.twitter.com/R_H_Ebright/status/14052391926286...
> The construction of novel chimeric SARS-related coronaviruses able to infect human cells and lab animals at WIV (1) was published with acknowledgment to NIH grant AI110964 (https://journals.plos.org/plospathogens/article?id=10.1371/j...) and (2) was reported to NIH under NIH grant AI110964 (https://reporter.nih.gov/search/0dVX_GElSEGDOsNMZq7qaQ/proje...)
So, yes, gain of function research was happening at WIV.