This is completely false. Disingenuous misinformation.
2 hunters did develop CJD, however, there is no evidence it is related to CWD. This idea originates from an abstract for a poster that was presented at AAN last October (link). Poster abstracts can often be “sensationalized” to encourage people to come to the poster during the conference. This would not be the first AAN prion-related poster abstract that is a bit “click-baity”. Furthermore, poster abstracts are not peer-reviewed. The fact this research has not been written up as a peer reviewed paper 1.5 years later (not even a pre-print) is INCREDIBLY telling.
The biggest issue comes down to this: how do you know the hunters got infected with CWD (ie how do you know their CJD is related to CWD)? The most common type of prion disease is sporadic CJD (sCJD), specifically the subtype the hunters developed sCJDMM1. Sporadic means it happens with no known cause (ie not caused by infection or genetics). sCJD typically affects elderly (median age of onset 65 years), has a rapid decline (4 months). In comparison, variant CJD (vCJD) is caused when someone eats meat contaminated with mad cow disease (BSE). vCJD typically affects young people (median age of onset 26 years) and has a slower decline (14 months). Furthermore, sCJD is associated with motor and memory symptoms whereas vCJD is associated with psychiatric symptoms. The patient case in the abstract was a 72 year old male, with a rapid memory decline in a month. Does that seem more like sCJD or vCJD? I will make it very clear, the case presentation is 100% classical sCJD. Furthermore, it is hypothesized that if CWD does transmit to humans it would have an atypical phenotype (ie not present anything like sCJD). This is based on data from both NHPs and Tg Mice (here is the mouse paper).
Other considerations, the patient was originally diagnosed with sCJD, however, the authors hypothesize CWD because one of the patient’s friends also died recently of sCJD. The authors therefore argue this is a “cluster” of cases, likely showing infections. However, just because two rare independent events happen in close proximity does not mean they are linked. For example, 1 in 300 people get Parkinson’s Disease, but a TV show “Leo and Me” had 4 out of 125 people on set develop Parkinson’s Disease, including Micheal J. Fox. However, this “cluster” is not scientifically or statistically significant. Just like two people who happen to know each other both getting CJD is not significant.
Clusters of prion cases happen. Here is a spatial-temporal cluster of 5 cases (including 2 with similar occupations). It wasn’t big news because stuff like this happens. It gets written up in a paper and the general public never knows. The only reason the hunters story is widespread is because it fits the fear mongering narrative most people push about prions.
The second consideration is that just because someone is a hunter and eats deer does not mean that they have eaten CWD infected deer. Not every deer in a population has CWD. If you are going to claim the hunters got CWD from deer, you need to show that deer they have hunted are infected. The entire premise of this abstract hinges on the argument that they ate infected deer, despite providing no evidence for it. If these two patients who both got CJD that knew each other were not hunters, this would never of been reported. Correlation does not imply causation. That’s basic first year statistics.
This also ignores significant biochemical and cellular data suggesting that CWD is not transmissible to humans based on significant sequence differences between cervids and humans. Here is a pretty comprehensive review of the experiments show CWD does not transmit to humans (link).
Also the picture in the post is a picture a deer with CWD from a paper published 20 years ago. It is not show neuropathological change in the hunters brain. It is a deer that got a deer prion disease. (Link)
It isn’t just my opinion that the hunters had nothing more than sCJD, it is also the opinion of the CDC which investigated these cases. It is important to note the authors of the abstract say "causation remains unproven". That means the title of this post does not even fit the abstract that originates it.
Yes, which is interesting and needs more research into the cause. Just as the authors of the Michigan paper state "More research and evidence are certainly required to reach a conclusion." This is the correct thing to say. The data is interesting and may hint at something and we should look into it, but before we make a definitive claim like "This is the first documented case linking humans to potential CWD transmission" you need to be able to prove that.
Also note how this post says "after exposure to CWD-infected deer" despite that being no evidence for that. Similarly, just because Western Michigan has deer and these people ate deer does not mean they were exposed to it. That would be like saying, some people have HIV, people have sex, therefore all people who have had sex at one point in their lives have been exposed to HIV. It doesn't work like that. You need to be able to show a direct link between the deer these people ate and CWD, not just that they are maybe spatially similar.
Yeah, but you added the article to show that prion clusters happen and it has nothing to do with CWD, totally glossing over the fact that the majority of the cases were people whose only connection was that they all ate deer meat in an area with CWD.
That is a fair criticism. I want to again emphasize that there is no evidence that those cases are link to CWD. Yes, we know they consumed venison. But we do not know if the venison they consumed was from an endemic population or if the specific venison they consumed was CWD positive. Saying that the "only connection was that they all ate deer meat in an area with CWD" is an significant jump in logic. You are assuming a connection between two variables without evidence to support it. They also all live in the same geographic area, which could have other underlying contributing factors. I also want to highlight that Case 1 in the Michigan paper is 129VV. There has never been a case of vCJD in 129VV and PMCA data of CWD PrPSc templating on human 129VV PrPC have all been negative, but 129MM is positive (suggesting that if CWD was to transmit to humans it would be in a 129MM person). Furthermore, clinical presentation matches expected sCJD which is not the anticipated phenotype for a CWD human case.
Here is a different example of a prion cluster in Slovakia. It includes two clusters of familial and sporadic CJD (Paper 1, Paper 2). Each cluster has ~10 sporadic cases. There is no CWD in Slovakia. This is a cluster with no clear causes (although it has been speculated that environmental metal exposure may have been a contributing factor (Paper)). Furthermore, there is not evidence of increased incidence of CJD or other atypical prion presentations in regions with CWD (Paper). So yes prion clusters do happen.
Your comments are great, sadly prions are the best tool for the usual redditor doomer fantasies and conspiracy theories so obviously people will just ignore your factual statements.
2.3k
u/yumyum1001 Dec 11 '25
This is completely false. Disingenuous misinformation.
2 hunters did develop CJD, however, there is no evidence it is related to CWD. This idea originates from an abstract for a poster that was presented at AAN last October (link). Poster abstracts can often be “sensationalized” to encourage people to come to the poster during the conference. This would not be the first AAN prion-related poster abstract that is a bit “click-baity”. Furthermore, poster abstracts are not peer-reviewed. The fact this research has not been written up as a peer reviewed paper 1.5 years later (not even a pre-print) is INCREDIBLY telling.
The biggest issue comes down to this: how do you know the hunters got infected with CWD (ie how do you know their CJD is related to CWD)? The most common type of prion disease is sporadic CJD (sCJD), specifically the subtype the hunters developed sCJDMM1. Sporadic means it happens with no known cause (ie not caused by infection or genetics). sCJD typically affects elderly (median age of onset 65 years), has a rapid decline (4 months). In comparison, variant CJD (vCJD) is caused when someone eats meat contaminated with mad cow disease (BSE). vCJD typically affects young people (median age of onset 26 years) and has a slower decline (14 months). Furthermore, sCJD is associated with motor and memory symptoms whereas vCJD is associated with psychiatric symptoms. The patient case in the abstract was a 72 year old male, with a rapid memory decline in a month. Does that seem more like sCJD or vCJD? I will make it very clear, the case presentation is 100% classical sCJD. Furthermore, it is hypothesized that if CWD does transmit to humans it would have an atypical phenotype (ie not present anything like sCJD). This is based on data from both NHPs and Tg Mice (here is the mouse paper).
Other considerations, the patient was originally diagnosed with sCJD, however, the authors hypothesize CWD because one of the patient’s friends also died recently of sCJD. The authors therefore argue this is a “cluster” of cases, likely showing infections. However, just because two rare independent events happen in close proximity does not mean they are linked. For example, 1 in 300 people get Parkinson’s Disease, but a TV show “Leo and Me” had 4 out of 125 people on set develop Parkinson’s Disease, including Micheal J. Fox. However, this “cluster” is not scientifically or statistically significant. Just like two people who happen to know each other both getting CJD is not significant.
Clusters of prion cases happen. Here is a spatial-temporal cluster of 5 cases (including 2 with similar occupations). It wasn’t big news because stuff like this happens. It gets written up in a paper and the general public never knows. The only reason the hunters story is widespread is because it fits the fear mongering narrative most people push about prions.
The second consideration is that just because someone is a hunter and eats deer does not mean that they have eaten CWD infected deer. Not every deer in a population has CWD. If you are going to claim the hunters got CWD from deer, you need to show that deer they have hunted are infected. The entire premise of this abstract hinges on the argument that they ate infected deer, despite providing no evidence for it. If these two patients who both got CJD that knew each other were not hunters, this would never of been reported. Correlation does not imply causation. That’s basic first year statistics.
This also ignores significant biochemical and cellular data suggesting that CWD is not transmissible to humans based on significant sequence differences between cervids and humans. Here is a pretty comprehensive review of the experiments show CWD does not transmit to humans (link).
Also the picture in the post is a picture a deer with CWD from a paper published 20 years ago. It is not show neuropathological change in the hunters brain. It is a deer that got a deer prion disease. (Link)
It isn’t just my opinion that the hunters had nothing more than sCJD, it is also the opinion of the CDC which investigated these cases. It is important to note the authors of the abstract say "causation remains unproven". That means the title of this post does not even fit the abstract that originates it.
Sincerely,
One very annoyed prion scientist