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ARS Home » Southeast Area » Athens, Georgia » U.S. National Poultry Research Center » Exotic & Emerging Avian Viral Diseases Research » Research » Publications at this Location » Publication #428029
Research Project: Intervention Strategies to Predict, Prevent, and Control Emerging Strains of Virulent Newcastle Disease Viruses

Location: Exotic & Emerging Avian Viral Diseases Research

Title: Chicken microRNA 26a-5p regulates replication of Newcastle Disease virus by direct targeting of the viral polymerase

Author
item Bakre, Abhijeet
item Mears, Megan

Submitted to: mBio
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 1/26/2026
Publication Date: N/A
Citation: N/A

Interpretive Summary: Newcastle disease outbreaks with virulent strains can cause significant morbidity and mortality and lead to substantial economic loss for both backyard and commercial poultry operations. Current vaccines can show sub-optimal protection against unrelated strains. Improving current ND vaccines depends on understanding the host immune response to infection better. In this manuscript, we identify multiple independent mechanisms via which a chicken small RNA miR-26a-5p can regulate replication of both vaccine and outbreak strains. Our data suggest that miR-26a-5p regulates the innate immune response following infection as well as directly binds to the viral polymerase gene inhibiting viral replication. These data identify new mechanisms via which existing vaccines can be improved and outbreak strains may be controlled.

Technical Abstract: Newcastle disease, caused by Orthoavulavirus javaense, is a significant threat to the poultry industry and outbreaks with virulent strains can lead to substantial economic loss. Studies to identify molecular pathways that can be used for intervention or reduce pathology are thus critical to mitigate losses due to ND. In this manuscript, we show that chicken miR-26a-5p can inhibit the replication of both lentogenic and velogenic pathotypes of OAVJ by acting via two distinct mechanisms, namely, by regulation of the host interferon response and by direct targeting of the viral polymerase gene. Mir-26a-5p upregulation inhibited replication of both lentogenic and velogenic OAVJ strains. Stable overexpression of miR-26a-5p led to down-regulation of multiple genes in the innate immune sensing and led to a small but significant increase in viral titer for a velogenic OAVJ strain. This study also identified a site for direct binding of mir-26a-5p to the OAVJ polymerase gene which was highly conserved across the majority of class II strains. Further, transfection of miR-26a-5p mimic following viral infection demonstrated a direct inhibition of polymerase transcripts while inhibitor transfection led to partial rescue of the miR-26a-5p mediated repression. These data identify new roles for chicken miR-26a-5p in regulating OAVJ replication.