Study points to active skin-cell role in rabies infection

Rabies researchers are sharpening the picture of what happens at the skin surface after exposure. A new Journal of Investigative Dermatology study found that human epidermal keratinocytes aren’t just passive bystanders: in lab models, they were susceptible to rabies virus infection, supported viral replication, mounted antiviral immune responses, and transmitted virus to neuronal cells across an intact microporous barrier. The work builds on earlier animal data from 2025 showing rabies-positive keratinocytes in experimentally infected mice and naturally infected dogs at suspected exposure sites, though that earlier study also suggested those skin findings may often reflect later-stage spread rather than the first step of infection. (sciencedirect.com)

Why it matters: For veterinary professionals, the study adds biologic plausibility to something clinicians and public health teams already take seriously: apparently minor scratches, superficial bites, or saliva contamination of broken skin can still pose rabies risk. It doesn’t change the core prevention message that prompt wound care and post-exposure prophylaxis remain essential, but it does help explain why superficial exposures shouldn’t be dismissed, especially when the source animal is a bat or an unvaccinated dog, cat, or other mammal under rabies suspicion. The strain-specific findings are also notable: bat-associated and attenuated strains infected keratinocytes more readily and triggered stronger immune activation than a dog-related strain, suggesting host-pathogen interactions at the skin level may vary by virus lineage. (sciencedirect.com)

What to watch: The next question is whether these keratinocyte-to-neuron mechanisms can be confirmed in vivo early after exposure, and whether they ultimately influence rabies risk assessment, wound management, or future biologic countermeasures. (sciencedirect.com)