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2015 ; 1
(ä): 15016
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Varicella zoster virus infection
#MMPMID27188665
Gershon AA
; Breuer J
; Cohen JI
; Cohrs RJ
; Gershon MD
; Gilden D
; Grose C
; Hambleton S
; Kennedy PG
; Oxman MN
; Seward JF
; Yamanishi K
Nat Rev Dis Primers
2015[Jul]; 1
(ä): 15016
PMID27188665
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Infection with varicella zoster virus (VZV) causes varicella (chickenpox), which
can be severe in immunocompromised individuals, infants and adults. Primary
infection is followed by latency in ganglionic neurons. During this period, no
virus particles are produced and no obvious neuronal damage occurs. Reactivation
of the virus leads to virus replication, which causes zoster (shingles) in
tissues innervated by the involved neurons, inflammation and cell death - a
process that can lead to persistent radicular pain (postherpetic neuralgia). The
pathogenesis of postherpetic neuralgia is unknown and it is difficult to treat.
Furthermore, other zoster complications can develop, including myelitis, cranial
nerve palsies, meningitis, stroke (vasculopathy), retinitis, and
gastroenterological infections such as ulcers, pancreatitis and hepatitis. VZV is
the only human herpesvirus for which highly effective vaccines are available.
After varicella or vaccination, both wild-type and vaccine-type VZV establish
latency, and long-term immunity to varicella develops. However, immunity does not
protect against reactivation. Thus, two vaccines are used: one to prevent
varicella and one to prevent zoster. In this Primer we discuss the pathogenesis,
diagnosis, treatment, and prevention of VZV infections, with an emphasis on the
molecular events that regulate these diseases. For an illustrated summary of this
Primer, visit: http://go.nature.com/14xVI1.
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