V — Varicella-Zoster Virus (VZV)
Varicella-zoster virus is an alphaherpesvirus with a linear double-stranded DNA genome. Primary infection causes varicella (chickenpox), after which the virus establishes lifelong latency in dorsal root and cranial nerve ganglia.
During primary infection, VZV infects respiratory epithelial cells, spreads via viremia in T cells, and seeds the skin, producing vesicular lesions. Like other herpesviruses, VZV encodes numerous immune evasion proteins that interfere with antigen presentation and interferon signalling.
Latency involves maintenance of the viral genome as an episome in neurons with highly restricted gene expression. Reactivation, often decades later due to waning cellular immunity, leads to herpes zoster (shingles), characterized by painful dermatomal rash.
Complications include postherpetic neuralgia, vasculopathy, encephalitis, and disseminated infection in immunocompromised hosts. VZV reactivation has also been implicated in stroke risk via viral infection of cerebral arteries.
Vaccination with live-attenuated (varicella) and recombinant subunit (zoster) vaccines reduces primary disease and reactivation. Research explores molecular mechanisms of latency, neuronal persistence, and immune correlates preventing reactivation.
Varicella-zoster virus is an alphaherpesvirus with a linear double-stranded DNA genome. Primary infection causes varicella (chickenpox), after which the virus establishes lifelong latency in dorsal root and cranial nerve ganglia.
During primary infection, VZV infects respiratory epithelial cells, spreads via viremia in T cells, and seeds the skin, producing vesicular lesions. Like other herpesviruses, VZV encodes numerous immune evasion proteins that interfere with antigen presentation and interferon signalling.
Latency involves maintenance of the viral genome as an episome in neurons with highly restricted gene expression. Reactivation, often decades later due to waning cellular immunity, leads to herpes zoster (shingles), characterized by painful dermatomal rash.
Complications include postherpetic neuralgia, vasculopathy, encephalitis, and disseminated infection in immunocompromised hosts. VZV reactivation has also been implicated in stroke risk via viral infection of cerebral arteries.
Vaccination with live-attenuated (varicella) and recombinant subunit (zoster) vaccines reduces primary disease and reactivation. Research explores molecular mechanisms of latency, neuronal persistence, and immune correlates preventing reactivation.