Genetic and vaccination studies reveal feather virus load as a potential biomarker for individual and flock-level protection against Marek’s disease in chicken

Authors: MARINA, HECTOR - Swedish University Of Agricultural Sciences; BAILEY, RICHARD - Roslin Institute; Mays, Jody; ITHURBIDE, MARIE - Université Paris-Saclay; CHASE-TOPPING, MARGO - Roslin Institute; CHENG, HANS - Retired ARS Employee; Dunn, John; DOESCHL-WILSON, ANDREA - Roslin Institute

Submitted to: Avian Pathology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 4/17/2026
Publication Date: 6/22/2026
Citation: Marina, H., Bailey, R., Mays, J.K., Ithurbide, M., Chase-Topping, M., Cheng, H., Dunn, J.R., Doeschl-Wilson, A. 2026. Genetic and vaccination studies reveal feather virus load as a potential biomarker for individual and flock-level protection against Marek’s disease in chicken. Avian Pathology. 1-60. https://doi.org/10.1080/03079457.2026.2661686.
DOI: https://doi.org/10.1080/03079457.2026.2661686

Interpretive Summary: Marek's disease is a significant problem for chickens, even with measures like good hygiene, vaccination, and choosing resistant chickens. The virus causing the disease keeps evolving, suggesting current methods are not fully effective. Vaccines help by reducing virus shedding, which decreases the number of sick and dead chickens. However, it was uncertain whether natural resistance provided similar protection to other chickens. To investigate, experiments were conducted using specific chickens to compare vaccination and natural resistance. These factors were assessed by observing virus shedding and outcomes when exposed to infected chickens. Chickens with natural resistance or vaccination were less likely to get sick and die. Vaccinated chickens shed significantly less virus in their feathers. Most exposed chickens became infected, indicating neither natural resistance nor vaccination fully prevented the spread. However, fewer chickens became severely ill or died when exposed to vaccinated birds shedding the virus. The timing of exposure also impacted the outcomes. Higher levels of virus in the feathers of infected birds or their cage mates correlated with increased sickness, death, and shedding in the exposed chickens. Measuring feather virus levels appears to be a good way to assess protection and could improve future breeding and vaccination strategies.

Technical Abstract: Marek’s disease (MD) remains a major threat to poultry, despite control efforts through biosecurity, vaccination, and genetic selection. Marek’s disease virus (MDV), the causative agent, continues to persist and evolve to increased virulence, indicating that current measures are suboptimal. While vaccination—even with ‘leaky’ vaccines—has been shown to reduce MD symptoms and mortality at the flock level by decreasing virus shedding, it is unclear whether genetic resistance offers similar indirect protection. Using natural transmission experiments in inbred layer chickens, we compared the effects of vaccination and genetic resistance on virus shedding and MD outcomes in both virus-inoculated shedder birds and unvaccinated MD susceptible contact birds. Shedder birds with genetic or vaccine-mediated resistance were less likely to develop disease and die, but only vaccinated shedders showed significantly reduced feather viral load (FVL). Nearly all contact birds became infected, suggesting that neither genetic resistance nor vaccination prevented transmission. However, significant reductions in symptomatic MD incidence and mortality were only observed in contacts exposed to vaccinated shedders. Exposure timing relative to shedders’ infection time also influenced contact outcomes. Process analyses and dose-response curves revealed that higher shedder or group mate FVL correlated strongly with MD incidence and mortality and shedding in contact birds. FVL emerged as a promising indicator for both individual and flock-level protection and could serve as a useful phenotype for future breeding and vaccination strategies aimed at reducing MDV transmission and limiting virulence evolution.