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herpes gestationis (HG) autoantibodies 322 herpesvirus-6 immunity
found in physiologic pregnancy. Direct immunofluorescence
may be used to demonstrate immunoglobulin G (IgG)
antibodies against the basement membrane zone in 30 to
50% of HG cases. By contrast, C3 is demonstrable at the skin
basement membrane zones in almost 100% of cases. Use of
the sensitive immunoblotting method permits identification
of antibodies against the hemidesmosome constituents of the
basement membrane zones in the skin of 90% of HG subjects.
herpes gestationis (HG) autoantibodies
Autoantibodies from patients with herpes gestationis (HG)
and bullous pemphigoid (BP) react with epidermal hemidesmosome
230- and 180-kDa proteins, respectively, helping to
anchor basal keratinocytes to the lamina densa of the basement
membrane. Although not present in normal pregnancy,
HG autoantibodies are found in 71 to 89% of positive HG
sera and in 47 to 53% of BP sera. Immunoglobulin G (IgG)
autoantibodies to the basement membrane zone (BMZ) are
revealed by direct immunofluorescence in 30 to 50% of
cases, whereas C3 is detected at the BMZ of perilesional
skin in approximately 100% of HG. With immunoblotting,
serum antibodies to heterogeneous hemidesmosomal components
of the BMZ can be detected in about 90% of HG
patients. The MCW-1 antigenic site that comprises a part
of the noncollagenous domain is believed to be involved
in subepidermal blister formation. Patients with HG and
their relatives face increased risk for development of other
autoimmune conditions such as Graves’ disease.
herpes simplex virus 1 and 2 (HSV-1 and HSV-2)
polyclonal antibody
An antibody used to identify specific and qualitative
localization of herpes simplex virus (HSV) types 1 and 2 in
formalin-fixed, paraffin-embedded or frozen tissue sections.
Herpesvirus.
Herpes simplex in the brain.
Double-stranded
linear DNA
Envelope
glycoproteins
Icosahedral
nucleocapsid
Tegument
proteins
HSV-1 is most often acquired during early childhood by nonvenereal
means and causes gingivostomatitis (fever blisters).
HSV-2 is usually acquired by venereal contact but can also
be acquired by a neonate from an infected mother’s genital
tract at the time of delivery. HSV-2 causes herpes genitalis.
herpes simplex virus immunity
The two related subtypes of herpes simplex virus (HSV) are
designated HSV-1 and HSV-2. The viruses are named human
herpesviruses 1 and 2, respectively. The immune response
to HSV has been investigated mainly in mouse, rabbit, and
guinea pig models. Genetic resistance of a host animal is a
result of several mechanisms, such as the effective killing
actions of macrophages and natural killer (NK) cells and
interferon synthesis. NK cells and interferon activity can
restrict an infection but cannot clear the virus, which depends
on the host-specific immune response. Both antibody and
T cell immunity are induced. Antibodies interact with the
virus, infected-cell glycoproteins, capsid proteins, and
selected infected-cell polypeptides. In mice, passively transferred
antibodies against HSV can protect from lethal doses
of the virus. Antibody alone is insufficient to clear virus
from the nervous system or the periphery; it may retard virus
spread through the nervous system. Antibody activities of
HSV-specific antibody in vitro include virus neutralization,
complement-mediated cytotoxicity, and antibody-dependent
cell-mediated cytotoxicity (ADCC). Reactivation and recurrence
or reinfection with HSV in humans often occurs in
the presence of high titers of neutralizing antibodies, which
reveals that the antibody has failed to protect. T cells are vital
in HSV infections. The cytotoxic T lymphocyte response to
HSV is mediated by CD8 + T lymphocytes in both humans
and mice. CD4 + major histocompatibility complex (MHC)
class-II-restricted lymphocytes are involved in the delayedtype
hypersensitivity response to HSV; CTL activity and T
cells help in antibody production. CD4 + T cells are critical
for clearance of the virus. The T H1 subset is protective. HSV
survives for many years in the host through establishment of
a latent infection without discernible protein expression. The
efficacy of avirulent or inactivated virus and subunit vaccines
has not been definitely established in human trials. Animal
trials have revealed that protection can be induced with glycoprotein
D using recombinant Salmonella introduced orally.
herpesvirus
A DNA virus family that contains a central icosahedral
core of double-stranded DNA and a trilaminar lipoprotein
envelope that is 100 nm in diameter and has a nucleus 30
to 43 nm in diameter. Herpesviruses may persist for years
in a dormant state. Six types have been described. HSV-1
(herpes simplex virus 1) can account for oral lesions such
as fever blisters. HHV-2 (human herpesvirus 2) produces
lesions below the waistline and is sexually transmitted. It
may produce venereal disease of the vagina and vulva, as
well as herpetic ulcers of the penis. HHV-3 (herpes varicella
zoster) occurs clinically as an acute form known as chickenpox
or as a chronic form termed shingles. HHV-4 (Epstein–
Barr virus), HHV-5 (cytomegalovirus), and HHV-6 (human
B cell lymphotrophic virus) are the other types.
herpesvirus-6 immunity
Humoral immune responses during primary infection
include an immunoglobulin M (IgM) response. Secondary
infection is associated with an increase in IgG titer as well
as a recrudescence of IgM reactivity. The humoral immune