An 18-year laboratory study led by researchers at the University of Calgary has found that prions from chronic wasting disease (CWD) — a fatal, always-progressive neurological disease of deer, elk, moose and other cervids — can infect non-human primates under experimental conditions. The finding, published in Science Advances and first reported by CIDRAP (the Center for Infectious Disease Research and Policy at the University of Minnesota), has reopened a long-running scientific debate: does CWD pose a genuine, if still unquantified, risk to humans who eat venison or handle infected animals?
The honest answer from the researchers and outside experts CIDRAP interviewed is: nobody knows yet, and the study itself does not settle it. What it does show is that the biological species barrier separating cervids from primates is not absolute — a result that keeps CWD on the list of prion diseases worth continued, serious surveillance, without confirming that any human has ever been sickened by it.
What prions are, and why CWD is different from most animal diseases
Prions are misfolded proteins that cause the body’s own normal proteins to misfold in turn, forming aggregates that progressively destroy brain tissue. Unlike viruses or bacteria, prions carry no genetic material, are extraordinarily resistant to standard sterilization and decontamination methods, and can persist in soil and the environment for years. Chronic wasting disease is one of a family of prion diseases that includes bovine spongiform encephalopathy (BSE, or “mad cow disease”) in cattle, scrapie in sheep, and Creutzfeldt-Jakob disease (CJD) in humans. CWD has been detected in free-ranging or farmed deer, elk and moose populations across dozens of U.S. states and Canadian provinces, and more recently in parts of Scandinavia and South Korea. It is always fatal in cervids and has no treatment or vaccine.
What the study actually found
The senior author, Hermann Schatzl, MD, PhD, of the University of Calgary, led a study in which researchers inoculated 18 female cynomolgus macaques with CWD prion preparations sourced from elk, mule deer and white-tailed deer, using both oral and intracerebral routes of exposure. Over a 7.5-year observation period, two of the macaques — one exposed orally and one intracerebrally — developed clinical signs consistent with prion disease, including unsteady movement and tremors.
Notably, standard diagnostic tests did not detect prions in these animals. Only highly sensitive amplification assays — protein misfolding cyclic amplification (PMCA) and real-time quaking-induced conversion (RT-QuIC) — picked up low-level infectious prion seeding activity. That distinction matters: it means the signal found was faint and technically difficult to detect, not a clear-cut, high-titer infection of the kind seen in natural CWD infection in cervids.
The real range of expert opinion — not resolved either way
CIDRAP’s reporting captures a genuine spread of expert judgment, not a consensus in either direction:
- Hermann Schatzl, the study’s senior author, argues the result is significant enough to revise blanket reassurance: “We clearly say that the concept that there is no zoonotic potential is likely not correct.” He is careful to frame this as evidence of potential risk under specific experimental circumstances, not proof of efficient, real-world transmission to humans.
- Olivier Andreoletti, a French prion researcher, pushes back on over-interpretation, stating that the study “does not demonstrate efficient transmission of CWD to macaques, nor does it show a classical prion disease phenotype,” and cautioning against extrapolating the result directly to human risk.
- Ryan Maddox of the U.S. Centers for Disease Control and Prevention notes that “CDC has found no evidence of CWD in people” to date, while also stressing that surveillance must continue precisely because prion diseases can take years to decades to produce symptoms — meaning an absence of confirmed human cases so far cannot be read as a guarantee of long-term safety.
- Peter Larsen, a CWD researcher at the University of Minnesota, expresses more concern about exposure levels in the human food supply, saying: “I worry that we’re underestimating the amount of positive venison being consumed.”
Read together, these views describe a field that treats the macaque result as a reason for continued vigilance and expanded surveillance — not as confirmation of an active human health emergency, and not as grounds for dismissing the risk either.
Why this matters for research integrity and public-health communication
This story is also a useful case study in how ambiguous, methodologically hedged findings should be communicated. The macaque result was detected only through highly sensitive molecular assays, in a small fraction of exposed animals, after years of observation — the kind of finding that resists a simple up/down headline. Research administrators, communications offices and public-health bodies covering emerging zoonotic and prion risks have a direct interest in resisting the temptation to either downplay a genuine, published, peer-reviewed signal or inflate it into settled fact. CIDRAP’s own framing — reporting the finding, the study’s real limitations, and the full range of named experts’ reactions rather than picking a side — is a useful model for how this kind of interspecies-transmission research should be reported.
What continued surveillance looks like
In practice, agencies including the CDC and USDA already recommend that hunters in areas with known CWD have harvested deer and elk tested before consumption, avoid eating meat from animals that test positive, and take precautions when field-dressing carcasses (gloves, minimizing contact with brain and spinal tissue, and using dedicated equipment). None of that guidance changes as a direct result of this study — it reflects a precautionary approach that predates it — but the new finding is likely to sharpen the case for maintaining and expanding both human and animal CWD surveillance programs while the underlying biology is worked out.
Frequently asked questions
Does this study prove CWD can infect humans?
No. It shows that under laboratory conditions, CWD prions produced a low-level, difficult-to-detect biological signal in 2 of 18 exposed macaques — a related primate species, not humans. Researchers CIDRAP spoke with, including the study’s own senior author, are explicit that this is evidence of potential zoonotic risk under specific conditions, not proof of efficient transmission to humans or evidence of an active human case.
Has CWD ever been confirmed to infect a human?
According to the CDC, as cited by CIDRAP, there is currently no confirmed evidence of CWD infection in humans. Surveillance continues in part because prion diseases can have incubation periods of years to decades, so an absence of confirmed cases to date does not rule out long-term risk.
What species were used in the study, and how were they exposed?
Researchers exposed 18 female cynomolgus macaques to CWD prion preparations derived from elk, mule deer and white-tailed deer, using both oral and intracerebral inoculation routes, and observed them for 7.5 years.
Why did experts disagree about the findings?
The disagreement centers on how much weight a faint, assay-dependent signal in a small number of animals should carry. Some researchers argue it is enough to revise assumptions of “no zoonotic potential”; others argue the study does not demonstrate efficient transmission or a classical prion disease pattern and caution against extrapolating to human risk. CDC’s position emphasizes continued surveillance rather than a revised risk estimate.
Primary source: CIDRAP, “After lab study finds interspecies spread of CWD prions, experts debate significance for humans,” July 30, 2026. Underlying study published in Science Advances, led by Hermann Schatzl, University of Calgary.
