Varicella (chickenpox) is associated with a viremia that results in a life-long association of the varicella-zoster virus (VZV) with neurons in sensory ganglia. VZV remains in a clinically inapparent (latent) form in these neurons because of the presence of VZV-specific immune responses that appear at the time of the childhood varicella infection. However, when these responses decline, as occurs with immune suppression, the latent VZV reactivates and causes herpes zoster (HZ). These same protective responses also decline naturally as part of the aging process.
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