Chronic wasting disease (CWD) has been spreading among deer in the United States, raising concerns about its potential to infect humans. However, a recent study suggests that CWD faces significant barriers to jumping to humans.
CWD is caused by prions, which are misfolded brain proteins, not by viruses or bacteria. A study using lab-grown miniature organs, called organoids, supports previous research showing that CWD prions do not infect human brain tissue. Researchers exposed brain organoids to high doses of prions from white-tailed deer, mule deer, and elk, and found no infections after 180 days. In contrast, organoids exposed to human prions causing Creutzfeldt-Jakob disease quickly became infected, suggesting a strong species barrier preventing CWD transmission to humans.
Bradley Groveman, a biologist at the National Institutes of Health’s Rocky Mountain Laboratories, noted that brain organoids provide a useful model for assessing the risk of CWD to humans. However, these organoids may not perfectly mimic human brains, potentially lacking features that make them susceptible to infection. Additionally, new prion strains could emerge that might infect humans.
Cathryn Haigh, a cell biologist at Rocky Mountain Laboratories, emphasized the importance of continued research to test new prion strains and monitor potential risks to humans.
The Spread of Chronic Wasting Disease
Deer infected with CWD are incurable. The disease, which affects deer, elk, moose, and other cervids, causes healthy brain proteins to misfold and clump together, killing brain cells and leading to symptoms like listlessness, stumbling, fearlessness, and drastic weight loss. Symptoms typically appear 18 to 24 months after infection.
Concerns about CWD’s risk to humans have grown due to its persistent spread across North America. CWD was recently reported for the first time in Indiana and California. The disease is now present in wildlife across 34 U.S. states, parts of Canada, South Korea, and northern Europe, significantly expanding since its first known case in 1967 in a captive deer in Colorado.
Debbie McKenzie, a prion biologist at the University of Alberta, noted an increase in the proportion of infected deer. In some populations, CWD prevalence exceeds 75%.
Hunters not testing their game increase the risk of infected deer meat reaching consumers. Cooking does not neutralize prions, unlike bacteria or viruses, so even cooked meat can pose a risk.
Lessons from Mad Cow Disease
The outbreak of mad cow disease, another prion disease, in the 1980s and 1990s highlighted the potential risks of prions to humans. While CWD was discovered before mad cow disease, the latter’s impact on humans raised awareness about CWD’s potential threat.
Research suggests prions have difficulty jumping between species. Studies in mice with human PrP proteins and macaques indicate that deer-to-human transmission of CWD is unlikely but not impossible. The risk remains a concern, especially since venison is commonly consumed in North America.
Vigilance and Future Research
News reports in April highlighted a case of fatal neurological disease in two hunters who had consumed deer meat from CWD-affected populations. However, these cases were likely caused by sporadic Creutzfeldt-Jakob disease, not CWD.
Ryan Maddox, an epidemiologist at the CDC, stated that no cases of CWD infection in humans have been reported to date. Despite this, the potential for new prion strains that could infect humans remains a concern. Understanding how prions misfold and infect different species is crucial for assessing the risk of CWD to humans.
McKenzie believes that while CWD could potentially jump to humans, such cases would likely be rare and not lead to an epidemic. Continued research and vigilance are essential to monitor and mitigate any potential transmission of CWD to humans.
