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PH-SD23

Viral skin infections

How viruses that infect the epidermis make warts, molluscum and herpes vesicles, why shingles follows one dermatome, and why the rashes of measles, rubella, parvovirus B19, roseola and hand, foot and mouth disease look and time as they do.

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  • 6 steps · 10 questions
  • 3D anatomy, affected parts marked

By the end, you can

  • Distinguish viruses that infect the epidermis directly from those that reach the skin through the blood, and relate each to the lesion it makes.
  • Explain how HPV, molluscum contagiosum virus and the herpesviruses change keratinocytes, producing koilocytes, molluscum bodies and multinucleated giant cells.
  • Explain how varicella-zoster virus becomes latent and reactivates as shingles in a dermatome, and why postherpetic neuralgia follows.
  • Relate the appearance and timing of the main childhood exanthems to how each virus spreads and how the immune response meets it.
  • Recognise the classic appearances, tests and numbers of viral skin infections, and explain how antivirals, destructive treatments and vaccines act on the mechanism.

What it is

Viral skin infections reach the skin in two ways. Some viruses are inoculated into the epidermis and make lesions where they enter, shaped by what they do to keratinocytes: human papillomavirus (warts), molluscum contagiosum virus and herpes simplex virus. Others reach the skin through the blood after infecting another organ, causing a widespread rash (an exanthem), sometimes with matching spots on the mucosa (an enanthem): measles, rubella, parvovirus B19, roseola, enteroviruses and chickenpox. Varicella-zoster virus does both: it reaches the skin through the blood as chickenpox and returns down a nerve as shingles.

3 types to tell apart
Proliferative (epidermis grows)
HPV and molluscum contagiosum virus make keratinocytes multiply, producing warts and pearly papules with little inflammation.
Cytolytic (keratinocytes die)
Herpes simplex and varicella-zoster viruses kill and fuse keratinocytes, producing vesicles; both stay latent in sensory ganglia and can return.
Exanthems (from the blood)
Measles, rubella, parvovirus B19, roseola, enteroviruses and chickenpox reach the skin through the circulation and cause widespread rashes.

US spelling: fibres → fibers.

Normal function

The epidermis as a target: maturing cells, vessels and nerves

Keratinocytes are born in the , the only layer that normally divides, and mature as they rise through the and layers: they stop dividing, fill with keratin, lose their nuclei and are shed from the about four weeks later. A virus that infects the epidermis must reach the basal cells, usually through a tiny abrasion, and its new particles are shed with the dead surface cells.

The epidermis has no vessels of its own. in the feed it by diffusion, and viruses circulating in the blood reach the skin through them. Inflammation and dilation of these small vessels underlie most viral rashes.

Sensory nerve fibres end in the dermis and among the cells of the epidermis. Their cell bodies lie far away, in the dorsal root ganglia beside the spinal cord or in cranial nerve ganglia, and each spinal nerve supplies one band of skin, a dermatome. Langerhans cells and T cells patrol the epidermis, and keratinocytes themselves make interferons when they sense viral nucleic acids.

Point to it on the model