Researchers at the Max Delbrück Center and University Medical Center Hamburg-Eppendorf mapped herpes simplex virus 1 infection across cell layers in hair-bearing skin organoids. Dermal fibroblasts accumulated high viral loads early, whereas basal keratinocytes and sensory neurons showed later infection. Spatial transcriptomics revealed local activation of IER3, antiviral IRF3, and spatially coordinated Tumor Necrosis Factor signaling.
Skin organoid model of HSV-1 infection
- ▪Human hair-bearing skin organoids provided by University Medical Center Hamburg-Eppendorf contain epidermal cells, dermal cells, hair follicles, and nerve-like cells, providing a three-dimensional model of herpes simplex virus 1 spread.
- ▪A study published in Science Advances by researchers at the Max Delbrück Center and University Medical Center Hamburg-Eppendorf traced how herpes simplex virus 1 infects human hair-bearing skin organoids.
Spread of HSV-1 across organoid cells
- ▪In human skin organoid infection tests, dermal fibroblasts carried large amounts of herpes simplex virus 1 early during infection.
- ▪Basal keratinocytes and hair follicle cells in skin organoids harbored lower viral amounts, with herpes simplex virus 1 reaching hair follicles and sensory neurons only later in the infection process.
Gene expression at the infection front
- ▪At the herpes simplex virus 1 infection front, dermal fibroblasts switched on the IER3 gene, while basal keratinocytes increased expression of the antiviral regulator gene IRF3.
- ▪Researchers combined tissue imaging with spatial transcriptomics to measure gene activity across individual cells at the leading edge of herpes simplex virus 1 infection in skin organoids.
Activation of Tumor Necrosis Factor signaling
- ▪Members of the Tumor Necrosis Factor family of signaling molecules were activated in a spatially coordinated manner during herpes simplex virus 1 infection in skin organoids.
- ▪Max Delbrück Center researcher Dr. Emanuel Wyler noted that Tumor Necrosis Factors activate the immune system and may significantly influence how effectively human bodies control herpes simplex virus 1 infection.
Neurological risks of HSV-1 infection
- ▪Herpes simplex virus 1 infects facial sensory nerve cells where it can remain dormant, but in rare instances it reaches the central nervous system to cause life-threatening brain inflammation.
- ▪Herpes simplex virus 1 is under scientific investigation for a potential role in Alzheimer's disease due to potential nerve cell damage from lifelong nervous system persistence.
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