The research assumes the conversion to a prion is direct, from one prion changing the conformation of normal protein, in isolation. But if there were some other cofactor necessary, like in CWD, maybe a co-infection producing antibodies which facilitated the change, then testing if the prion alone will do it will show it won’t, whereas if it were combined with the unknown cofactor, it would.
They openly say in the paper they don’t know 100% that direct transformation in isolation is the mechanism of disease, then say they tested if it would produce disease, it would not, so therefore it is safe.
I would say the lack of caution in the result is outright malpractice. You have two hunters who ate a CWD deer who got CJD. You’d think they would err on the side of safety.
I studied CJD, Scrapie, and Kuru in microbiology years ago and there were many hypothesis about the transmission of the disease. We called them “slow viruses” back then. Biochemistry has evolved to identify the culprit but there still have’t been studies to characterize the prions replication and identify cofactors necessary to infect an individual. It could be genetics. In the early 80’s we had a product made from rumens of sheep and were fed to cattle...I suspect it was the origin of “Mad Cow” disease. In Europe “Mad Cow” spread into the beef herds and before it was correctly identified they fed the carcasses to hogs...and the hogs had the “mad cow” but since their lifespans were short no one identified it for quite some time and those consuming the hogs developed CJD like syndromes. I wouldn’t eat any animal that tested positive for CWD. The study that is mentioned that CWD is safe was done on only 10 macaques and 10 spider monkeys. The ten spider monkeys died of CWD and the macaques lived and died of natural causes. I wouldn’t place my bets on a study with just these results.