How does VZV cause lesions?
Activation of host cyclin-dependent kinases in VZV-infected fibroblasts. VZV infects quiescent cells such as dermal fibroblasts (HFFs) to cause skin lesions.
What is VZV vasculitis?
Varicella zoster virus (VZV) infection of intra- and extracranial arteries (VZV vasculopathy) may be associated with a granulomatous vasculitis characterized by vessel wall damage and transmural inflammation, with multinucleated giant cells and/or epithelioid macrophages.
What are three diseases caused by varicella zoster virus?
Postherpetic neuralgia, acute encephalitis, aseptic meningitis and myelitis are the most frequent diseases and have been recorded both in association with herpes zoster and in the absence of a cutaneous rash.
What type of skin lesion is varicella?
Varicella in Unvaccinated Persons It progresses rapidly from macular to papular to vesicular lesions before crusting. Lesions are typically present in all stages of development at the same time. The rash usually appears first on the chest, back, and face, then spreads over the entire body.
What does a high varicella zoster IgG mean?
A positive IgG result indicates the presence of antibodies to varicella zoster virus. – The test cannot distinguish between past infection and current infection though, so a positive result could indicate active infection and not immunity.
What are the life cycle stages of varicella-zoster virus?
It is responsible for an infection that manifests as separate illnesses in two phases of the human life cycle: 1) a primary infection, varicella (chickenpox), typically in childhood; and 2) a secondary herpes zoster (HZ) infection (shingles) through reactivation of the latent virus in the central nervous system (CNS).
How do you describe a varicella rash?
The classic symptom of chickenpox is a rash that turns into itchy, fluid-filled blisters that eventually turn into scabs. The rash may first show up on the chest, back, and face, and then spread over the entire body, including inside the mouth, eyelids, or genital area.
How does VZV become latent?
Both viruses are typically acquired early in life, during which time both viruses gain access to ganglia where they become latent. Reactivation from latency results in replication and shedding of infectious virus, which ensures the virus is transmitted to a naive population [1].
Why is varicella more severe in adults?
This childhood disease is harder to fight the older you get. Everybody knows that you need to get the chickenpox when you’re young.
What is the pathophysiology of VZV vasculopathy?
VZV vasculopathies can complicate zoster or varicella and are caused by productive viral infection in cerebral arteries. The important features of VZV vasculopathy are summarised in the panel. Unlike most cases of acute viral encephalitis, VZV vasculopathy is often chronic and protracted.
When is VZV vasculopathy considered in the workup of polyneuritis cranialis?
VZV vasculopathy should be considered when cranial nerve lesions occur in mono- or polyneuritis cranialis syndromes with or without rash. Venous Sinus Thrombosis
What are the diagnostic criteria for varicella-zoster virus (VZV) vasculopathy?
VZV vasculopathy should be suspected in individuals, particularly if immunocompromised, who have had a stroke or aneurysm with: (1) a recent history of varicella or zoster, (2) recurrence of unclear cause with or without rash, or (3) unclear etiology and absence of stroke risk factors.
Does VZV affect the extracranial circulation in giant cell arteritis?
Recently, several studies emerged indicating that VZV vasculopathy can also affect the extracranial circulation, including temporal arteries (TAs) from patients with giant cell arteritis (GCA).