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Neurovirulence of varicella and the live attenuated varicella vaccine virus
Journal article   Peer reviewed

Neurovirulence of varicella and the live attenuated varicella vaccine virus

Corey Horien and Charles Grose
Seminars in pediatric neurology, Vol.19(3), pp.124-129
09/2012
DOI: 10.1016/j.spen.2012.02.006
PMCID: PMC3419367
PMID: 22889542
url
https://www.ncbi.nlm.nih.gov/pmc/articles/3419367View
Open Access

Abstract

Varicella-zoster virus (VZV) is a neurotropic herpesvirus, which can cause a variety of complications during varicella infections. These range from meningoencephalitis to polyneuritis to retinitis. After primary VZV infection, VZV enters the dorsal root ganglia in a latent state. Reactivation from latency leads to zoster. Zoster ophthalmicus in particular can in turn lead to involvement of the cerebral arteries and subsequent stroke. The velocity of VZV is 13 cm per day, as virus travels from ganglion to skin. The live attenuated varicella vaccine virus is markedly less neurovirulent than the wild type virus. Nevertheless, a few cases of herpes zoster due to the vaccine virus have been documented. Usually, herpes zoster occurs in the same arm as the vaccination, often 3 or more years after vaccination. Thus, herpes zoster in a vaccinee often represents a reactivation of vaccine virus that was carried to the cervical dorsal root ganglia from a site of local replication in the arm. Finally, the role of autophagy during VZV is discussed. Autophagosome formation is a prominent feature in the skin vesicles during both varicella and herpes zoster. Therefore, autophagy is one of the innate immune mechanisms associated with VZV infection in humans.
 Varicella encephalitis Herpes zoster Stroke Autophagy

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