Investigating Antiviral Immune Mechanisms in Bats 4145
Abstract Description Bats (order Chiroptera) are known carriers of lethal human viruses yet rarely exhibit disease symptoms. Research suggests bats have evolved unique mechanisms to tolerate viruses, reducing disease severity through long-term co-evolution. Studying these adaptations could provide critical insights for developing antiviral therapies, which remain challenging due to viral diversity, rapid evolution, and host toxicity. Bat immunology is a relatively new field. Early studies show that bats possess immune cell functions similar to those in humans and other mammals, alongside evidence of a dampened innate inflammatory response. However, how bats maintain immune tolerance while regulating virus replication remains poorly understood. Our research addresses this gap using in vitro models with the recombinantly recovered H18N11 influenza A virus in immortalized bat epithelial lung cells. We assess infection kinetics—including adhesion, entry, replication, and release—and compare them to human and mouse epithelial cells infected with species-specific influenza A viruses. Transcriptomics and RNAseq are employed to identify innate immune transcripts and differentially expressed proteins in response to infection. By isolating antiviral proteins and their effector mechanisms, we aim to uncover therapeutic insights inspired by bats’ evolved immune responses. Leveraging bat’s unique immune phenotype could lead to innovative antiviral stratgies, strengthening pandemic preparedness. Topic Categories Viral Immunology (VIR)
Authors
- Hannah K. Frank (ORCID: https://orcid.org/0000-0002-4507-181X)
- Jonathan D. Rosen (ORCID: https://orcid.org/0000-0001-6396-4219)
- James B. McLachlan (ORCID: https://orcid.org/0000-0001-7741-391X)
Institutions
- Tulane University (US)
Publication Details
- Journal
- The Journal of Immunology
- Published
- 2025-11-01
- DOI
- https://doi.org/10.1093/jimmun/vkaf283.1863
- Primary Topic
- interferon and immune responses
- Type
- article
- Field-Weighted Citation Impact
- 0.00