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Herpes zoster (shingles) is a
recurrent, painful, erythematous vesicular eruption caused by the
reactivation of latent varicella-zoster virus in an individual who had
chickenpox
years earlier.
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Adults with shingles may transmit the
virus to children and cause
chickenpox.
During the latent phase, the virus
resides in the dorsal root spinal ganglion or the cranial nerve
ganglion.
On reactivation, the virus spreads from
the ganglia along sensory nerves to peripheral nerves of the sensory
dermatomes.
Attacks of shingles produce cutaneous
lesions that resemble varicella.
In shingles, however, the eruptions are
limited to one or more sensory dermatomes, and the vesicles or bullae
may be few.
Shingles is painful, especially in
older people, in contrast to the painless vesicles of children with
chickenpox.
Eventually the scales over the vesicles
slough, and symptoms remit until another attack.
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Herpes Simplex Virus Infection
Herpes
folliculitis is a rare manifestation of herpes virus infection and it
is often misdiagnosed. Diagnostic criteria are not well established,
only 24 patients being reported in the literature. Recently it has
been suggested that herpetic folliculitis is more common in infections
with varicella zoster (VZV) than in those with herpes simplex viruses
(HSV-1 and -2).In biopsy specimens taken from herpes virus infections,
involvement of follicular units is more commonly encountered in VZV
infections compared with HSV infections. Early in the course, herpes
folliculitis presents as lymphocytic folliculitis devoid of epithelial
changes considered to be diagnostic of herpes virus infections.
Exclusive involvement of follicles is rather typical of zoster.Herpes
folliculitis: clinical, histopathological, and molecular pathologic
observations.
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Molecular studies of Varicella zoster virus.Rev
Med Virol. 2006 Jul-Aug;16(4):225-50
VZV is a highly
cell-associated member of the Herpesviridae family and one of the
eight herpesviruses to infect humans. The virus is ubiquitous in
most populations worldwide, primary infection with which causes
varicella, more commonly known as chickenpox. Characteristic of
members of the alphaherpesvirus sub-family, VZV is neurotropic and
establishes latency in sensory neurones. Reactivation from
latency, usually during periods of impaired cellular immunity,
causes herpes zoster (shingles). Despite being one of the most
genetically stable human herpesviruses, nucleotide alterations in
the virus genome have been used to classify VZV strains from
different geographical regions into distinct clades. Such studies
have also provided evidence that, despite pre-existing immunity to
VZV, subclinical reinfection and reactivation of reinfecting
strains to cause zoster is also occurring. During both primary
infection and reactivation, VZV infects several PBMC and skin cell
lineages. Difficulties in studying the pathogenesis of VZV because
of its high cell association and narrow host range have been
overcome through the development of the VZV severe combined
immunodeficient mouse model carrying human tissue implants. This
model has provided a valuable tool for studying the importance of
individual viral proteins during both the complex intracellular
replication and assembly of new virions and for understanding the
underlying mechanism of attenuation of the live varicella vaccine.
In addition, a rat model has been developed and successfully used
to uncover which viral proteins are important for both the
establishment and maintenance of latent VZV infection. |
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