TY - JOUR
T1 - Age-based host response to Turkey arthritis reovirus in commercial Turkeys in the presence of maternally derived antibodies
AU - Khatiwada, Saroj
AU - Ngunjiri, John
AU - Boley, Patricia A.
AU - Yadav, Kush K.
AU - Ghorbani, Amir
AU - Abundo, Michael
AU - Lee, Carolyn M.
AU - Poelstra, Jelmer W.
AU - Lee, Chang Won
AU - Gharaibeh, Saad
AU - Rajashekara, Gireesh
AU - Kenney, Scott P.
N1 - This project is supported by Agriculture and Food Research Initiative Competitive Grant no. 2021-67015-34465 from the USDA National Institute of Food and Agriculture.
PY - 2025/12
Y1 - 2025/12
N2 - Background: Turkey arthritis reovirus (TARV) causes arthritic lameness in market-age turkeys. Since 2011, highly pathogenic TARV strains have caused significant economic losses in the turkey industry due to increased culling, reduced market weights, and decreased carcass quality, necessitating more effective control measures. Autogenous vaccine prevention strategies have been inefficacious partly due to a limited understanding of age-related susceptibility of turkeys to TARV. This study investigated age-related host and gut microbiota responses to TARV infection in commercial turkeys derived from vaccinated breeder hens. Poults with known maternally derived antibody titers were orally challenged with TARV O’Neil strain at 1-, 3-, and 7- weeks of age (WOA) and monitored for cloacal virus shedding, gastrocnemius tendon viral tropism, tendon inflammation, weight gain, and changes in gut microbiota. Results: A transient TARV-induced weight gain suppression was evident in poults infected at 1- and 3- WOA during the first 3 weeks post-infection. Age-dependent variations in cloacal viral shedding, virus isolation from tendons, and tendon inflammation severity were also observed. There was significant dissimilarity in ileal and cecal bacterial communities between mock and infected groups, but the effect of age of infection was unclear. Conclusions: Age dependent host response was observed to TARV based on cloacal virus shedding, weight gain suppression and viral tendon tropism. Our study also indicates that maternally derived antibodies appeared insufficient to prevent virus translocation to the tendons and subsequent pathological changes. This study lays the groundwork for future investigations of better vaccines/vaccination strategies and alternative preventive measures. Importance: Turkey arthritis reovirus (TARV) causes lameness due to arthritis and tenosynovitis, commonly in market-age turkeys, resulting in significant economic losses. As a control strategy, the turkey industry used autogenous vaccines, prepared from field TARV isolates in breeder hens, to protect the poults in the early stage of life through maternally derived antibodies (MDAs). This study establishes the level of protection provided by MDAs in young poults with age-based responses to TARV O’Neil reovirus strain. Additionally, this study reveals the dynamics of gut dysbiosis in infected poults at different timepoints, paving the way to ground-breaking investigations into gut microbiome modulation interventions that could potentially improve vaccine efficacy and reduce virus transmission and disease severity.
AB - Background: Turkey arthritis reovirus (TARV) causes arthritic lameness in market-age turkeys. Since 2011, highly pathogenic TARV strains have caused significant economic losses in the turkey industry due to increased culling, reduced market weights, and decreased carcass quality, necessitating more effective control measures. Autogenous vaccine prevention strategies have been inefficacious partly due to a limited understanding of age-related susceptibility of turkeys to TARV. This study investigated age-related host and gut microbiota responses to TARV infection in commercial turkeys derived from vaccinated breeder hens. Poults with known maternally derived antibody titers were orally challenged with TARV O’Neil strain at 1-, 3-, and 7- weeks of age (WOA) and monitored for cloacal virus shedding, gastrocnemius tendon viral tropism, tendon inflammation, weight gain, and changes in gut microbiota. Results: A transient TARV-induced weight gain suppression was evident in poults infected at 1- and 3- WOA during the first 3 weeks post-infection. Age-dependent variations in cloacal viral shedding, virus isolation from tendons, and tendon inflammation severity were also observed. There was significant dissimilarity in ileal and cecal bacterial communities between mock and infected groups, but the effect of age of infection was unclear. Conclusions: Age dependent host response was observed to TARV based on cloacal virus shedding, weight gain suppression and viral tendon tropism. Our study also indicates that maternally derived antibodies appeared insufficient to prevent virus translocation to the tendons and subsequent pathological changes. This study lays the groundwork for future investigations of better vaccines/vaccination strategies and alternative preventive measures. Importance: Turkey arthritis reovirus (TARV) causes lameness due to arthritis and tenosynovitis, commonly in market-age turkeys, resulting in significant economic losses. As a control strategy, the turkey industry used autogenous vaccines, prepared from field TARV isolates in breeder hens, to protect the poults in the early stage of life through maternally derived antibodies (MDAs). This study establishes the level of protection provided by MDAs in young poults with age-based responses to TARV O’Neil reovirus strain. Additionally, this study reveals the dynamics of gut dysbiosis in infected poults at different timepoints, paving the way to ground-breaking investigations into gut microbiome modulation interventions that could potentially improve vaccine efficacy and reduce virus transmission and disease severity.
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U2 - 10.1186/s12917-025-04525-1
DO - 10.1186/s12917-025-04525-1
M3 - Article
C2 - 39994714
AN - SCOPUS:85218702903
SN - 1746-6148
VL - 21
JO - BMC Veterinary Research
JF - BMC Veterinary Research
IS - 1
M1 - 96
ER -