An alternative theory of herpes-simplex recurrence and a possible role for prostaglandins.
Reactivation of herpes-simplex is thought to require stimulation of latent virus in the sensory ganglion before the virus travels to the skin and causes a lesion. An alternative theory is proposed whereby virus is often released from the ganglion to form microfoci of infection in the skin but these are usually eliminated. Physiological changes in the skin, perhaps induced by prostaglandins, occasionally allow lesions to develop.
D000818:Animals; D005724:Ganglia / Q000382:microbiology*; D006561:Herpes Simplex / Q000150:complications* / Q000382:microbiology; D006801:Humans; D051379:Mice; D011453:Prostaglandins / Q000502:physiology*; D011458:Prostaglandins E / Q000494:pharmacology; D011817:Rabbits; D012008:Recurrence; D018139:Simplexvirus / Q000187:drug effects; D012867:Skin / Q000294:innervation / Q000382:microbiology*; D014276:Trigeminal Nerve / Q000382:microbiology; D014774:Virulence; D014779:Virus Replication / Q000187:drug effects
D011453:Prostaglandins; D011458:Prostaglandins E