Magnus Nygård Osnes
maos.bsky.social
Magnus Nygård Osnes
@maos.bsky.social
Researcher at the Norwegian Veterinary Institute | Genomic epidemiology, Phylodynamics, Population dynamics, Computational biology |
The epidemic trajectories are sensitive to the mechanistic parameter assumptions. Varying them within reasonable ranges we get the similar shapes, but shifting prevalences and timings
| 10/12
September 18, 2025 at 11:24 AM
We observe a temporally confined peak followed by fade out in Scenario 1, stabilizing high prevalence in Scenario 2, and slow peak followed by slow decline in Scenario 3. | 9/12
September 18, 2025 at 11:24 AM
Averaged over simulations we see rapid selection and genotype frequencies substantially altered in all scenarios after 40 years across all scenarios. | 8/12
September 18, 2025 at 11:22 AM
A cool result is that when PRNP affects on susceptibility only, the epidemic progresses through a peak followed by a rapid decline, but when less susceptible PRNP genotypes with a longer disease duration is included, the prevalence peaks and remains high. 7/12
September 18, 2025 at 11:22 AM
We simulated for 80 yrs, starting with 1 infected adult male. Many runs die out stochastically—even if R₀ > 1 — e.g. when early cases die by natural mortality or is hunted before transmitting the disease. Outbreak probabilities differ substantially between scenarios. | 6/12
September 18, 2025 at 11:21 AM
We simulated CWD dynamics under 4 PRNP mechanisms:
• No effect
• Susceptibility (S1).
• Susceptibility + shedding duration (S2).
• Susceptibility + duration + clinical shedding level (S3).
We based assumptions on literature on closely related species with similar PRNP alleles |
5/12
September 18, 2025 at 11:20 AM
CWD susceptibility is tied to PRNP gene variation. But exactly how PRNP genotypes alter susceptibility, shedding duration & shedding level is still unknown. For a good overview of Cervidae PRNP variants see: doi.org/10.1186/s135...
| 4/12
September 18, 2025 at 11:19 AM
We built a stochastic transmission model for CWD in SimInf, matching the reindeer demography, hunting, and dynamics at Hardangervidda – the only wild herd where contagious CWD is thought to be present in Europe | 3/12
September 18, 2025 at 11:18 AM
Our first WiLiMan project paper is out #wilimanid! 🎉 We modelled how host genetics might shape Chronic Wasting Disease (CWD) dynamics in wild reindeer (Rangifer tarandus). Read here: doi.org/10.1016/j.ec... (Photo: Olav Strand/NINA) | 1/12
September 18, 2025 at 11:16 AM
Here’s the “mother phylogeny” of Norwegian isolates spanning nearly a decade. Too many resistance patterns to unpack here, but AZM, CFM, and CIP phenotypes/mechanistic markers are shown in the columns. | 8/13
September 15, 2025 at 1:28 PM
Zooming in using phylodynamics, ST-1580 comprises two BAPS groups: 7 and 1, which we estimate to have diverged far back in time. One of the clades is the female-associated (BAPS7), and the other is associated with men (BAPS1). The “female” clade is the one in explosive growth! | 7/13
September 15, 2025 at 1:27 PM
We used Bayesian Analysis of Population Structure (BAPS) to delineate lineages and followed these to determine if specific lineages changed dramatically in frequency before and after the pandemic.
| 4/13
September 15, 2025 at 1:26 PM
From ~1,704 cases in Norway in 2019, the incidence fell to ~555 in 2021 under lockdown. But by 2023, it skyrocketed to 2,985. One of our major questions was which lineages fueled this dramatic resurgence? | 3/13
September 15, 2025 at 1:25 PM