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Home > D. General pathology > Infectious diseases > varicella-zoster virus

varicella-zoster virus

Tuesday 17 March 2009

Digital slides

- UI:931 - Varicella

Two conditions-chickenpox and shingles-are caused by varicella zoster virus (VZV). Acute infection with VZV causes chickenpox; reactivation of latent VZV causes shingles (also called herpes zoster).

Chickenpox is mild in children but more severe in adults and in immunocompromised patients. Shingles is a source of morbidity in elderly and immunosuppressed persons.

Like HSV, VZV infects mucous membranes, skin, and neurons and causes a self-limited primary infection in immunocompetent individuals.

Also like HSV, VZV evades immune responses and establishes a latent infection in sensory ganglia.62 In contrast to HSV, VZV is transmitted in epidemic fashion by aerosols, disseminates hematogenously, and causes widespread vesicular skin lesions.

VZV infects neurons and/or satellite cells around neurons in the dorsal root ganglia and may recur many years after the primary infection, causing shingles.

Localized recurrence of VZV is most frequent and painful in dermatomes innervated by the trigeminal ganglia, where VZV is most likely to exist in a state of latency. In contrast to numerous recurrences of HSV, VZV usually recurs only once, most frequently in immunosuppressed or elderly persons.


The chickenpox rash occurs approximately 2 weeks after respiratory infection and travels in multiple waves centrifugally from the torso to the head and extremities.

Each lesion progresses rapidly from a macule to a vesicle, which resembles a dewdrop on a rose petal. On histologic examination, chickenpox vesicles contain intranuclear inclusions in the epithelial cells like those of HSV-1.

After a few days, most chickenpox vesicles rupture, crust over, and heal by regeneration, leaving no scars. Traumatic rupture of some vesicles with bacterial superinfection may lead to destruction of the basal epidermal layer and residual scarring.

Shingles occurs when VZVs that have long remained latent in the dorsal root ganglia after a previous chickenpox infection are reactivated and infect sensory nerves that carry viruses to one or more dermatomes.

There, VZVs cause vesicular lesions, which are differentiated from chickenpox by the often intense itching, burning, or sharp pain because of the simultaneous radiculoneuritis.

This pain is especially strong when the trigeminal nerves are involved; rarely, the geniculate nucleus is involved, causing facial paralysis (Ramsay Hunt syndrome).

In the sensory ganglia, there is a dense, predominantly mononuclear infiltrate, with herpetic intranuclear inclusions within neurons and their supporting cells.

VZV also causes interstitial pneumonia, encephalitis, transverse myelitis, and necrotizing visceral lesions, particularly in immunosuppressed patients.