Alberta whitetails carrying two copies of the 96S variant of the prion protein gene tested CWD positive 1 time in 138, compared with 55 times in 1,045 for whitetails carrying no copy. That gap makes no difference for a hunter at the check station, because deer with 96S still tested positive and nobody can tell a deer's genotype in the field. Our rule is to turn in the head of every deer you kill in a CWD zone and consider that deer untested until the result returns, whatever its genes.
IMain Finding
One of 138 Whitetails Carrying Two 96S Copies Was Positive
Whitetails carrying one copy landed between those groups with 13 positives among 899. Bubac and colleagues sequenced the gene using ear tissue from deer whose heads hunters submitted to Alberta's CWD surveillance program from 2014 to 2017, then published their findings in Ecology and Evolution in 2025. The variant replaces glycine with serine at position 96 of the prion protein, which geneticists call G96S. FDR's guide to the hours after the shot explains sampling, cooling and carcass waste.
IITest Odds
No-Copy Whitetails Had 7.75 Times the Positive-Test Odds of Two-Copy Whitetails
An initial round of 575 whitetails (67 positive) and 660 mule deer (202 positive) found 14 variable sites in the whitetail gene and 8 in the mule deer gene. G96S was the only site that separated positive from negative whitetails, with 96S appearing less often among positives and more often among negatives.
Compared with whitetails carrying two 96S copies, whitetails carrying no copy had an odds ratio of 7.75 (confidence interval 1.04 to 57.95). The genotype table showed positive tests in 5.3% of no-copy deer and 0.7% of two-copy deer. Deer carrying one copy had an odds ratio of 2.09 (interval 0.27 to 16.53). The first interval sits barely above 1 and the second includes it, and both span a wide range because positives were few. The authors nevertheless suggest that a single 96S copy "may confer some limited resilience to infection."
In every genotype males tested positive more often than females. Among whitetails carrying no 96S copy, positive tests came from 47 of 594 males and 8 of 450 females. An additive model in which each 96S copy lowers positive-test odds another step and a model grouping one-copy deer with no-copy deer both fit the data, with a slightly better fit for the additive model.
Swipe table to see every column
| Genotype | Males (positive) | Females (positive) | All deer (positive) | Percent positive |
|---|---|---|---|---|
| 96S/96S, two copies | 81 (1) | 57 (0) | 138 (1) | 0.72% |
| G96/96S, one copy | 489 (12) | 410 (1) | 899 (13) | 1.45% |
| G96/G96, no copy | 594 (47) | 450 (8) | 1,045 (55) | 5.26% |
| Total | 1,164 (60) | 917 (9) | 2,082 (69) | 3.31% |
IIIPlace and Time
96S Increased With Time and Was Higher Near First Detections in Does
The team next sequenced another 1,612 whitetails. The map model drew on 35 wildlife management units with at least 15 deer each, totaling 2,012 deer. Among females the 96S frequency (the share of gene copies carrying 96S) ranged from 0.111 to 0.457 across units and dropped with distance from the two areas where Alberta first found CWD. Units west and south of the endemic area had less 96S, and the authors suggest deer there "may be at somewhat greater risk of the disease."
Males had a narrower range of 0.172 to 0.433, with no distance pattern and only a weak link to years since CWD first appeared in the unit. The authors suggest that dispersing males and heavier male harvest may blur a local signal, while females remain near their birthplace.
To examine change over time the authors used a 2005 Alberta frequency of 0.225 in 98 deer from an earlier study by Wilson and colleagues. The authors projected that frequency forward six generations under four published estimates of selection strength, using 2 years per generation. Their forecast for 2017 ranged from 0.230 to 0.292, while the 854 whitetails sampled in 2017 measured 0.281. Both studies sampled Unit 151 well and its frequency rose from 0.197 in 33 deer to 0.297 in 37 deer, slightly above the forecast.
Swipe table to see every column
| Area | 2005 frequency | 2017 frequency | Against the forecast |
|---|---|---|---|
| Alberta sample | 0.225 (98 deer) | 0.281 (854 deer) | Inside the forecast of 0.230 to 0.292 |
| Unit 151 | 0.197 (33 deer) | 0.297 (37 deer) | Just above the forecast |
Our read is that even if selection drives the change it moves slowly. In the Alberta samples the share of gene copies carrying 96S rose from 22.5% to 28.1% in 12 years, while half of the genotyped whitetails still had no copy.
IVDisease Remains
Deer With 96S Still Get CWD and May Carry It Longer
According to the authors, none of the known variants of the prion protein gene offers full resistance to CWD, and the Alberta genotype table records positive tests in both carrier groups. In experimental infections cited by the authors, Race and colleagues found that 96S extended incubation and pushed back onset without stopping disease. Miller and colleagues found that deer with one copy first tested positive at about the same time as deer with none but lived longer, while deer with two copies tested positive later and survived longest.
Our read is that living longer with CWD still leaves a deer carrying CWD, so genotype cannot replace a test result.
The authors note that breeding for 96S has already begun in farmed whitetail herds, and Pilot and colleagues found that 96S rose over 17 years in farmed herds in Alberta and Saskatchewan. The authors point to possible fitness costs for deer carrying one or two copies, giving fawn mortality as an example. The authors also caution that over time the CWD agent could adapt to infect deer with these genotypes more easily.
VMule Deer Findings
Study Found No Prion Gene Link to CWD in Alberta Mule Deer
The authors note that mule deer have Canada's highest CWD infection rate, yet no gene link appeared in the 660 Alberta mule deer studied. Just 2 of the 8 variable sites in the mule deer gene could be checked for a link. The team suspected that the other 6 sites were linked to a pseudogene (a second gene copy) and could not confirm genotypes at those sites. Disease status showed no link to either tested site. The codon 225 variant linked to slower disease in Wyoming and Colorado mule deer did not appear, and Wilson and colleagues also found no variation there in western Canada. The authors describe that gap as unexplained.
Our read is that Alberta mule deer hunters get no genetic good news from this data set, and the mule deer test covers just two sites.
VIFew Cases
Sixty-Nine Positives Drive the Whole Whitetail Finding
This observational study cannot show that 96S prevents infection. In the genotype table only 69 whitetails tested positive and just 1 carried two copies. The map model used 35 positives, and units with more positives supplied more samples as well (correlation 0.495). The authors say the small number of cases limits their choice between gene models.
Harvest samples leave out deer that die of CWD before the season, and the authors note that selection on those deer remains unseen. Surveillance then focused on southeastern Alberta, while the 2005 baseline came from a separate study of 98 deer. Our read is that distance from the first detection offers a rough yardstick, since FDR's Missouri paper found that CWD jumps to new ground there.
NOTES AND SOURCES
- Source: Bubac and colleagues 2025, Ecology and Evolution, prion protein gene variation and CWD in Alberta white-tailed deer and mule deer.
- Also: Wilson and colleagues 2009, prion gene variation in western Canadian deer (the 2005 baseline of 98 deer).
- Scope: Hunter-submitted white-tailed deer and mule deer from Alberta's CWD surveillance program, 2014 to 2017, mostly from southeastern Alberta. The first round sequenced 575 whitetails (67 CWD positive) and 660 mule deer (202 positive), and 1,612 more whitetails were sequenced later. The genotype table totals 2,082 whitetails with 69 positives, and the map model covers 35 wildlife management units.
- Method: Figures are quoted from the paper's text and tables. Percent positive by genotype and by sex, genotype shares and the change in 96S frequency were computed by FDR from the printed counts and frequencies. Odds ratios and intervals are as printed, and the paper does not state the confidence level of its intervals.
- Limits: Observational association in hunter-harvested deer. It does not show that 96S prevents infection.
- Limits: Only 69 positive whitetails in the genotype table and 1 positive 96S/96S deer, so the odds ratio intervals are wide and the one-copy interval includes 1.
- Limits: The 2005 baseline comes from a different study (Wilson and colleagues 2009) of 98 deer.
- Limits: Surveillance at the time focused on southeastern Alberta. Deer that die of CWD before the hunting season are missing from harvest samples.
- Limits: Units with more positives also contributed more samples (r = 0.495).
- Limits: No PRNP variant is known to give complete resistance. 96S/96S and G96/96S deer tested positive.
Fully Drawn Research is an independent data analysis desk, not affiliated with any state wildlife agency, transportation agency, mapping provider or outfitter. Fully Drawn Research is an independent data and analysis desk. This paper summarizes published research and adds FDR's reading of what it means for hunters. Figures are quoted from the studies linked in the text, and figures we computed from them are labeled as ours.
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