Wednesday, May 27, 2026

Odocoileus virginianus PRNPsequencing reveals AF (Q95G96/H95G96) advantage over AC (Q95G96/Q95S96) against chronic wasting disease

  Odocoileus virginianus PRNPsequencing reveals AF (Q95G96/H95G96) advantage over AC (Q95G96/Q95S96) against chronic wasting disease 

Research Open access 

Published: 26 May 2026 Volume 57, article number 84, (2026) 

Veterinary Research Aims and scope Submit manuscript 

Odocoileus virginianus PRNP sequencing reveals AF (Q95G96/H95G96) advantage over AC (Q95G96/Q95S96) against chronic wasting disease 

Evan W. London, Alfred L. Roca, Yasuko Ishida, Tooba Latif, Jan E. Novakofski & Nohra E. Mateus-Pinilla 

Abstract

Chronic wasting disease (CWD) is a highly transmissible spongiform encephalopathy impacting cervids. Variations in the prion protein gene (PRNP), encoding the prion protein (PrP), influence disease progression and susceptibility. Protein sequence is a key determinant of PrP strains and their capacity for interspecies transmission. Sequencing PRNP in white-tailed deer has revealed non-synonymous polymorphisms impacting disease—c.285A > C (Q95H) and c.286G > A (G96S). Previous PRNP amplification protocols misclassified homozygous and heterozygous deer due to allelic dropout by a widely used forward primer. We resequenced 586 deer previously classified as homozygous using a redesigned primer (designated Ov-PRNP-F2) and found 128 heterozygotes. Subsequently, we sequenced additional CWD-positive and CWD-negative deer using Ov-PRNP-F2 to correct for dropout and then estimated PrP variant susceptibility and CWD risk using 778 CWD-positive and 3,070 CWD-negative deer from 22 Illinois counties, the largest PRNP sequence dataset to date. Animals encoding PrP variant combination C (96S) and F (95H) were the least susceptible to CWD (OR = 0.03, p < 0.001) compared to deer encoding two copies of PrP variant A 95Q;96G. A novel finding is that deer encoding a single copy of PrP 95H were less susceptible to CWD compared to those with a single copy of PrP 96S (OR = 0.40, p < 0.001). The results support using genotyping methods to map susceptibility to CWD across the landscape, focusing on PrP variant frequencies to improve CWD epidemiological risk models.

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A strategy targeted at removing PrP variant A animals would seemingly minimize CWD susceptibility, but may have unintended impacts, and such selection could contribute to the emergence of new strain types [53]. Furthermore, animals with PrP variant combinations including C and F could serve as silent carriers indirectly transmitting prions to the environment, which may potentiate spread.


“However, during the past seven years, Illinois saw a rapid increase in prevalence rates – up to 9.2% in 2025 – and a continued spread southward into central Illinois. The expanded geographic distribution, along with growing fatigue among cooperating landowners and the public, prompted IDNR to suspend its targeted culling efforts.”

Illinois Chronic Wasting Disease Update: Spring 2026

New detections prompt suspension of sharpshooting operations

This year, chronic wasting disease (CWD) was detected in the state’s deer herd in three new counties: Effingham, Scott, and Stark. Effingham and Scott join Adams County as the first documented cases outside of the leading edge of the northern Illinois CWD endemic region, resulting in 28 counties where the disease has been detected.

These recent detections are clear indicators that the disease has expanded beyond IDNR’s capacity to manage it effectively through a long-term sharpshooting program. After a valiant 23-year effort by biologists to control CWD in Illinois’ deer herd, IDNR will suspend its targeted culling (sharpshooting).

Illinois’ free-ranging deer herd is an incredibly valuable and cherished public resource and the heart of outdoor culture in the state. Protecting the health of the herd has always been the goal of IDNR’s CWD management program. CWD is fatal in every case and can impact white-tailed deer populations.

The disease was first detected in Illinois deer in 2002 when it was discovered in Boone County. Since 2003, IDNR has employed active CWD management through sharpshooting, coupled with liberalized hunting opportunities and baiting restrictions, to lower prevalence in affected areas and slow the spread of the disease.

The program IDNR developed earned national recognition for its ability to slow the spread. These efforts kept CWD prevalence low in Illinois – below 2% – and confined to the northern part of the state for almost an entire generation of deer hunters

However, during the past seven years, Illinois saw a rapid increase in prevalence rates – up to 9.2% in 2025 – and a continued spread southward into central Illinois. The expanded geographic distribution, along with growing fatigue among cooperating landowners and the public, prompted IDNR to suspend its targeted culling efforts.

About the Disease

CWD can be transmitted between deer and is caused by misfolded proteins called a prion, which can damage brain and nerve tissue in deer, elk, moose, and other members of the Cervid family.

CWD has been documented in 36 states and five Canadian provinces. Illinois joined other fish and wildlife agencies, the federal government, and universities in providing research and knowledge about the disease. Through management efforts and collaboration, experts have learned a great deal about the disease.

All available information indicates CWD prevalence will continue to increase and the disease will spread into new areas. White-tailed deer population declines and age-structure impacts have been documented in areas of high CWD prevalence. A relatively small increase in harvest and removal of deer at the local level can help keep CWD prevalence low.

Although the Centers for Disease Control and Prevention have not linked CWD to human transmission, they recommend against eating meat from CWD-positive deer. Hunters are encouraged to have their deer tested and avoid consuming brain, spinal cord, eyes and other tissues known to harbor the CWD agent.

Next Steps

IDNR staff will continue to monitor CWD within the state, provide sampling opportunities for hunters, and engage with the public to help address management of the disease.

IDNR also will host public open houses with hunters and landowners around the state this summer to update them on the status of the disease in Illinois and encourage continued vigilance and testing when harvesting deer.

Illinois hunters and landowners have been valuable partners from the beginning and will continue to play a vital role in CWD monitoring and management by:

Continuing to hunt and harvest deer

Encouraging deer hunting on private property

Increasing the number of deer taken – particularly antlerless deer – in and around areas with CWD

Having harvested deer tested for CWD

Acknowledgements

The IDNR thanks the many partners and organizations that continue to help battle this disease: the cooperating hunters and landowners, US Fish and Wildlife Service, USDA Wildlife Services, the Illinois Natural History Survey, Wildlife Veterinary Epidemiology Laboratory, the SIU Cooperative Research Laboratory, and the Illinois Department of Agriculture.


Chronic wasting disease is a fatal disease of the central nervous system in deer and elk. CWD was first detected in a suspect adult female deer from northwest Boone County in 2002. Since then, 185,896 wild deer have been sampled statewide, and 2,748 individual deer tested positive for CWD.

Between July 1, 2024 and June 30, 2025, IDNR's Wildlife Disease Program identified 539 CWD-positive deer in 25 Illinois counties, including Adams, Boone, Bureau, Carroll, Cook, DeKalb, DuPage, Ford, Grundy, Jo Daviess, Kane, Kankakee, Kendall, Lake, LaSalle, Lee, Livingston, Marshall, McHenry, Ogle, Peoria, Putnam, Stephenson, Will and Winnebago.



PROBLEM STATEMENT 6B: REVEAL GENETICS OF PRION DISEASE SUSCEPTIBILITY.

Greater frequency of chronic wasting disease in free-ranging elk genetically tolerant to disease progression raises concerns related to prion transmission and strain evolution.

Animal Disease Research Unit, Pullman, Washington

Genetic variations in the prion protein gene of Rocky Mountain elk do not confer complete resistance to fatal infection by chronic wasting disease. However, elk carrying one or two copies of the amino acid leucine (L) variant at position 132 of the prion protein (132L*, where * is either M for methionine or L) survive much longer than 132MM elk. An ARS researcher in Pullman, Washington, in collaboration with researchers at the University of Wyoming, the University of California at Davis, the National Park Service, and the Animal and Plant Health Inspection Service, found a higher frequency of 132L* elk in areas of Wyoming with high infection rates, consistent with the expected positive effect of prolonged survival on reproduction. However, the frequency of chronic wasting disease infection in 132L* elk was also higher than previous estimates. To improve the long-term management of native elk populations, these findings underscore the importance of determining the effects of prolonged infection on disease transmission from 132L* elk and the potential for driving prion strain diversification.


Research Project: Elucidating the Pathobiology and Transmission of Transmissible Spongiform Encephalopathies

Location: Virus and Prion Research

Title: Update: CWD genetic resistance project at NADC

Author item Cassmann, Eric item Greenlee, Justin Submitted to: North American Deer Farmer Publication Type: Trade Journal Publication Acceptance Date: 11/5/2023 Publication Date: 11/15/2023 Citation: Cassmann, E.D., Greenlee, J.J. 2023.

Update: CWD genetic resistance project at NADC. North American Deer Farmer. P. 83. Interpretive Summary: Technical Abstract: In March of 2020, we began a study to examine the susceptibility of whitetail deer with rare prion protein genotypes to chronic wasting disease (CWD). In the sequence of amino acids that make up the deer prion protein, there are several locations that are variable. These variations are sometimes called polymorphisms. In the data collected from depopulations, whitetail deer with certain prion gene polymorphisms were not positive for CWD. In 2019, Dr. Nick Haley published a paper that showed H95/S96, HH95, and S96/K226 deer from depopulated herds in the US were not CWD positive. Based on the overall low number of deer with these genotypes () we’re unable to determine if they were resistant to CWD or if there were too few deer with these genotypes to be statistically represented in the positive cases. It’s also possible that they could be partially susceptible with longer incubation times than deer with generic (wild type) prion genotypes. Samples gathered at depopulation represent a snapshot of the herd. It is possible these rare genotypes were exposed, but had not yet accumulated abnormal prion protein to a level detectable by the detection methods used. The NADC susceptibility study was initiated to help answer these questions.

We studied deer with polymorphisms at 3 amino acid locations (codons): 95, 96, and 226. Wild type deer are QQ95GG96QQ226. Whitetail deer with wild type prion genotypes were inoculated with CWD and co-housed with other whitetail deer (contact deer) that had rare prion protein genotypes. The genotypes of contact deer included QH95GS96QQ226, QH95GG96QK226, QQ95GS96QQ226, QQ95SS96QQ226, Q95GS96QK226, and QQ95GG96KK226 (bolded text indicates a prion gene polymorphism).

During the first year, we collected feces, saliva, nasal swabs, skin, blood, and rectal biopsies from the inoculated and contact deer to determine if deer are CWD positive and the period of CWD shedding. After the first year, we started collecting rectal biopsies annually on the contact deer, but all other samples are still collected every three months.

Eight out of ten (8/10) inoculated deer developed clinical signs for CWD and tested positive after necropsy (Figure 1). The average time from inoculation to euthanasia of these eight inoculated deer was 23 months.

Two inoculated deer are still on-study; one of these deer has tested positive for CWD on rectal biopsy IHC.

To date, two deer from the contact group have developed CWD clinical signs and tested positive (Figure 2). The positive deer from the contact group had the GS96QK226 and KK226 genotypes.

We have detected CWD prions in rectal biopsies with IHC in three other contact deer as of October 2023. Their prion genotypes are GS96, QH95GS96, and GS96QK226.

As the experiment continues, we hope to answer 2 main questions. (1) Are there any prion protein polymorphisms that make deer resistant to CWD, and (2) what are the CWD shedding dynamics in deer with detectable CWD. One potential outcome of the study would be identifying genotypes with very long incubation periods that, while susceptible to CWD, still could be used to manage CWD.


Update: CWD genetic resistance project at NADC 1) Are there any prion protein polymorphisms that make deer resistant to CWD, and (2) what are the CWD shedding dynamics in deer with detectable CWD. One potential outcome of the study would be identifying genotypes with very long incubation periods that, while susceptible to CWD, still could be used to manage CWD.


Another potential and likely outcome of this study, imo, is that genotypes developed with very long incubation, could therefore, if released into the wild, could help spread cwd even further, exposing even more wild species, and surrounding environments, for even longer periods of time, due to the longer incubation, a terrible potential outcome, one that must be avoided at all cost, imo…terry

SATURDAY, APRIL 11, 2026 

Chronic Wasting Disease CWD TSE PrP, Cervid, Genetic Manipulation, Unforeseen Circumstances 


FRIDAY, MAY 01, 2026

Oklahoma House Bill 3270 FAILED, Great News for Hunters and Wildlife


SUNDAY, MAY 04, 2025

Texas Senate Bill 2651 establishment of a pilot program to breed deer resistant to CWD TSE Prion, what could go wrong?


FRIDAY, FEBRUARY 21, 2025

LEGISLATING CWD TSE Prion, Bills to release Genetically Modified Cervid into the wild, what could go wrong?


MONDAY, JUNE 09, 2025

Genetic Approaches and Tools to Prevent, Control, and Eradicate Transmissible Spongiform Encephalopathies 2024 Annual Report ARS Research


FRIDAY, OCTOBER 31, 2025

Captive Cervid and the Economic Burden of Chronic Wasting Disease CWD TSE Prion?

The economic burden of ignoring CWD would be far greater, imo, with time, if no cervid were left, or just a select few, if the environment/property was so exposed and saturated with CWD, that you couldn’t sell it, you couldn’t grow crops because of the soil saturation of the CWD, water tables saturated with CWD, saturation of hay, grains, from crops uptake on said property, cervid meat saturated from Cervid CWD, remember, You cannot cook the TSE prion disease out of meat, In fact new data now shows that exposure to high temperatures used to cook the meat increased the availability of prions for in vitro amplification. So, what Do we do, how many humans and animals do we continue to expose, continue to saturate with the CWD TSE Prion, how many will become infected, what about friendly fire, ie iatrogenic exposure to the CWD TSE Prion, do we just ignore all science, all transmission studies that confirm all this is very possible, is this what we want to leave our children and grandchildren? Just because no documentation of human TSE Prion disease from CWD has not been documented, does not mean it cannot happen, or has not already happened. It’s kinda hard to state categorically that CWD has transmitted to humans, or not, when no diagnostic diagnosis criteria is set up for any such event, especially for iatrogenic, that I am aware of…terry

Captive Cervid and the Economic Burden of Chronic Wasting Disease CWD TSE Prion?


SATURDAY, SEPTEMBER 27, 2025 

Illinois IDNR Report 539 CWD positive deer in 25 counties Between July 1, 2024, and June 30, 2025 


SATURDAY, MAY 16, 2026 

Captive CWD Indemnity Program or Entitlement Program? 


Distribution of Chronic Wasting Disease in North America APRIL 11, 2025


Texas CWD TSE Prion Cases Climb To 1,377 Cases Detected to date May 19, 2026



Terry S. Singeltary Sr.

posted by Terry S. Singeltary Sr. at 10:55 AM

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