DISCUSSION
The role of EBV as a potential inducer or exacerbator of autoimmune
blistering disorders in children is debated, while there seems to be
sufficient evidence to support its role as an infectious trigger factor
in adults. In fact, DNA sequences of EBV have been found in 5% of skin
biopsies of adult patients affected by bullous pemphigoid (BP).6F. Drago et al. detected DNA sequences of HHV, including EBV, in 27% of
skin samples, further supporting the potential role of herpesviruses as
elicitors of an autoimmune response in genetically predisposed patients.
Regarding PV, the evidence supporting the role of EBV as a trigger is
scarce4.
In their study, Sagi et al. found no significant difference in EBV
antibodies between patients with autoimmune blistering diseases
(comprehending both BP and PV patients) and healthy controls. The
authors concluded that their findings suggest a minor contribution of
EBV in autoimmune blistering
disorders.3Finally, to date, there are no reports of other autoimmune bullous
diseases (such as linear IgA bullous dermatosis or epidermolysis bullosa
acquisita) associated with EBV in adult patients.
On the other hand, EBV is more commonly associated with paraviral skin
eruptions. In adolescents and young adults, primary EBV infection
frequently results in infectious mononucleosis. In approximately 5% of
patients affected by mononucleosis, the viral infection is associated
with skin eruption characterized by heterogeneous lesions (such as
macular, petechial, urticarial, scarlatiniform of erythema
multiforme-like
lesions).7A transient erythematous, maculopapular eruption involving trunk and
upper extremities is also common in patients affected by mononucleosis
who received antibiotic therapy in the previous 10
days.8In children, EBV is one of the most common infectious agents associated
with Gianotti-Crosti syndrome (GCS). GCS (also referred to as papular
acrodermatitis of childhood) is an acute, autolimited eruption involving
acral skin sites. Clinically, GCS is characterized by symmetrical,
monomorphic papular lesions tending to be asymptomatic. The most
frequently involved sites are cheeks, buttocks, extensor aspects of
arms, hands and thighs. Viral antigens have not been demonstrated in
skin on ultrastructural or immunohistochemical
studies.9GCS can rarely manifest with vesiculobullous lesions: a bullous form of
GCS also falls within the differential diagnosis of paraviral bullous
eruptions.
To date, there is only one case report of an EBV-induced autoimmune
bullous disease in a child. Baldari et. al. reported the case of a
3-year-old girl developing chronic bullous disease of childhood (a
variant of linear IgA bullous dermatitis) following recent EBV
seroconversion. The authors hypothesized that EBV was able to stimulate
the patient’s immune system (through immortalization of B lymphocytes
and activation of T lymphocytes) ultimately leading to the development
of an autoimmune
disease.10Case reports of autoimmune bullous diseases in children induced by other
Human-Herpes viruses (such as HSV and VZV) were also
reported.2,11