Latent infection

A restricted range of viruses, most being in the Herpesviridae family (HSV, varicella-zoster virus ( VZV ), EBV, and  CMV ), give rise to latent  infections within the  host, as a result of evading immune clearance during the  primary  infection (which can  be acute or inapparent). During latent infections virus replication is curtailed as a result of viral regula- tory mechanisms, significantly suppressing virus production; in fact for HSV and VZV no new virus is produced during latency. Intermittently, virus replication may be reacti- vated and virus production is resumed (recurrence), possibly leading to clinical symp- toms (recrudescence) that may be similar or different to those observed during primary infection. Both HSV and VZV produce a primary infection in skin and mucosal cells, but a latent infection within neurons and both can reactivate from a latent state many times during the life of an individual. HSV is found latent within the neurons of the trigeminal or sacral ganglia between periods of reactivation, when recurrence can produce the typical painful cold sore lesions on the mouth or genitals. It is not fully understood what happens to reactivate the virus at the cellular level, although a number of stimuli includ- ing menstruation, exposure to UV light, and stress are responsible for initiating it. A very different clinical syndrome may result from the reactivation of VZV. The primary infec- tion produces chickenpox, whereas reactivation is associated with the development of shingles, a localized area of extremely painful vesicles that can in some cases remain for many weeks. Additionally, some patients suffer from very severe post-herpetic neuralgia that can persist for months or years.