Animal Models and Pharmacology of Herpetic and Postherpetic Pain.
Behavioral Neurobiology of Chronic Pain
Current topics in behavioral neurosciences, February 2014
Kuraishi Y, Sasaki A, Yasushi Kuraishi, Atsushi Sasaki
Bradley K. Taylor, David P. Finn
Varicella-zoster virus (VZV) causes varicella upon primary infection and subsequently becomes latent in the sensory ganglia. Reactivation of latent VZV in the sensory ganglion results in herpes zoster, which usually begins with pain and dysesthesia. Pain that persists long after healing of the rash is termed postherpetic neuralgia. VZV inoculation into rats induces mechanical allodynia and thermal hyperalgesia without causing herpes zoster. As with VZV, herpes simplex virus 1 (HSV1) is an alphaherpesvirus. HSV1 also becomes latent in the sensory ganglia after primary infection, and reactivation of latent HSV1 in the sensory ganglion results in herpes simplex. HSV1 inoculation into mice causes zoster-like skin lesions together with mechanical allodynia and mechanical hyperalgesia. A marked difference between the two rodent models is whether the herpes virus proliferates in the nervous system after inoculation. VZV-inoculated rats are useful for investigating mechanical allodynia induced by latent infection with herpes virus. HSV1-inoculated mice are useful for investigating mechanical allodynia induced by the proliferation of herpes virus in sensory neurons and for assessing the effects of acute herpetic pain on the incidence of postherpetic allodynia.
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