CWD is increasingly spreading across the United States

CWD in Deer Threatens Human Health, Experts on High Alert

United States: Chronic wasting disease (CWD) has been proliferating among cervid populations within the United States, inciting apprehension regarding its potential transmission to humans. Nonetheless, recent research indicates that the pathway for CWD to infiltrate human biology is considerably arduous.

The agent responsible for CWD is not a conventional pathogen like a virus or bacterium but a misfolded brain protein known as a prion. Novel investigations employing lab-cultivated mini-brains, or organoids, corroborate earlier studies, demonstrating that CWD prions fail to infect human neural tissue.

In a study published in the June 2024 edition of Emerging Infectious Diseases, organoids exposed to substantial doses of prions from white-tailed deer, mule deer, and elk remained uninfected over a 180-day period. Conversely, organoids exposed to human prions responsible for Creutzfeldt-Jakob disease quickly succumbed to infection, suggesting a robust species barrier against CWD transmission to humans, according to sciencenews.org.

“This model offers valuable insights into the actual risk,” asserted Bradley Groveman, a biologist at the National Institutes of Health’s Rocky Mountain Laboratories in Hamilton, Montana.

However, brain organoids are not perfect replicas of actual brains and might lack certain characteristics that would make them vulnerable to infection. New prion strains could potentially emerge, including some that might facilitate the binding of deer prions to healthy human brain proteins.

To vigilantly monitor the potential risk to humans, researchers must continue gathering evidence and testing new prion strains on organoids and through other experimental methods, says Cathryn Haigh, a cell biologist at the same institution. “Declaring human infection as impossible may never be feasible.”

Proliferation of a Fatal Disease

Deer afflicted with CWD face inevitable demise, as no cure exists. The prions causing CWD induce a normal brain protein called PrP to deform into an abnormal configuration. These distorted proteins aggregate, leading to neuronal death and symptoms such as lethargy, unsteady gait, loss of fear of humans, and severe weight loss. Symptoms typically manifest 18 to 24 months post-infection, as highlighted by sciencenews.org.

The continuous spread of CWD across North America has heightened concern about the risk posed by prions from deer, elk, and moose to humans. On April 5, CWD was first reported in Indiana, and on May 6, officials in California announced the state’s inaugural cases in two wild deer. To date, CWD has been identified in wildlife across 34 US states, parts of Canada, South Korea, and northern Europe—a significant rise since the initial case in a captive deer in Colorado in 1967.

Moreover, the prevalence of infected deer has increased, notes Debbie McKenzie, a prion biologist at the University of Alberta in Edmonton, Canada. “Previously, only about 1 in 100 or 1 in 1,000 deer were infected… now some deer populations exhibit CWD prevalence exceeding 75 percent.”

If hunters do not test their game, the likelihood of infected venison reaching consumers rises. Cooking does not neutralize prions as it does bacteria or viruses, so even cooked meat could pose a hazard.

Historical Insights and Current Research

The mad cow disease outbreak in the 1980s and 1990s, when people consumed meat from infected cattle, brought attention to CWD. Although CWD was discovered earlier, concerns about its threat to humans were initially minimal.

However, the realization that a bovine prion could infect humans and cause disease highlighted the potential risk says Haigh. “This awareness has now extended to another disease in animals we consume,” the reports by sciencenews.org mentioned.

Previous research has indicated that prions may struggle to jump between certain species. Experiments with genetically modified mice carrying the human PrP protein have suggested that while transmission to humans is possible, it is less likely than transmission of prions from cattle. Studies involving macaques, often used as human analogs, also hint that deer-to-human transmission of CWD is improbable.

Nevertheless, the possibility of prion transmission from wildlife to humans remains a significant concern, particularly given the consumption of venison in North America. Vigilance is crucial to detect any potential transmission early, despite some alarms being false.

In April, media reports highlighted a case presented at the American Academy of Neurology meeting in Denver, describing fatal neurological disease in two hunters who consumed deer meat from a CWD-endemic area. However, both likely succumbed to Creutzfeldt-Jakob disease, which can occur sporadically, according to the report and the U.S. Centers for Disease Control and Prevention.

“To date, there have been no reported cases of CWD in humans,” confirms epidemiologist Ryan Maddox of the CDC in Atlanta.

Barriers to Prion Transmission

While the mad cow prion-infected hundreds starting in 1994—taking a decade or more to manifest symptoms—the transmission barrier to humans was significantly high. Despite millions being exposed to contaminated beef during the 80s and ’90s outbreak, as of 2022, only 178 cases of Creutzfeldt-Jakob disease linked to infected meat have been reported in the UK and 55 globally.

The factors contributing to susceptibility remain unclear. It is plausible that those infected were exposed to an extremely high dose, or their brain PrP protein had an optimal shape for interaction with bovine prions, says McKenzie. “Other contributing factors to susceptibility must also exist.”

Prion strains, which twist PrP proteins differently, also play a role. Groveman explained that the misfolding pattern of prions can prevent cross-species infection. Understanding how deer prions fold and interact could elucidate what might potentially infect humans or other animals, as sciencenews.org outlined.

However, elucidating prion structures is more challenging than studying normal PrP proteins, complicating the investigation of prion diseases’ cross-species potential.

At least five prion strains cause CWD, each infecting different cervid species. “We lack a comprehensive understanding of strain generation in animals,” McKenzie added. Lab studies indicate that some strains may infect other animal species, yet no cases of CWD have been documented outside cervids in the wild.

Thus, while brain organoid studies suggest that current strains may not pose significant threats to humans, new, riskier strains could emerge. “CWD potentially jumping to humans remains a possibility,” McKenzie states, though she anticipates such instances to be rare. “An epidemic is unlikely.”

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