Skin organoids reveal how herpes simplex virus spreads between cells

Researchers at the Max Delbrück Center and University Medical Center Hamburg-Eppendorf have traced in skin organoids, how herpes simplex virus 1 infection progresses among neighboring skin cells, deepening our understanding. The work was published in Science Advances.

Most people think of herpes simplex virus 1 (HSV-1) as a mere cosmetic problem: The virus can cause outbreaks of cold sores on the lips or face, which usually heal on their own within two weeks. But HSV-1 infection can be more sinister. The virus infects sensory nerve cells in the face, where it usually remains dormant. In rare cases, it travels to the central nervous system and causes life-threatening brain inflammation. HSV-1 is also being investigated for potentially playing a role in Alzheimer's disease - its lifelong persistence in our nervous system may eventually damage nerve cells.

Dr. Emanuel Wyler, a scientist in the RNA Biology and Posttranscriptional Regulation lab at the Max Delbrück Center, has had a longstanding interest in understanding how the virus causes disease. Now he and collaborators at University Medical Center Hamburg-Eppendorf (UKE) have traced step by step how HSV-1 infects the multiple layers of skin cells. Using human hair-bearing skin organoids as a model, the researchers mapped how the virus spreads and which signaling molecules cells release to their neighbors upon being infected.

Tracking HSV-1 in 3D skin

Skin is built like a layered sandwich. The protective outermost layer is the epidermis, which primarily consists of keratinocytes. Beneath it sits the dermis, a support layer rich in fibroblasts. Hair follicles pass through these layers, which also contain sensory nerve fibers.

How neighboring cells react to infection 

Source:

Max Delbrück Center for Molecular Medicine in the Helmholtz Association

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