Expression of Herpes Simplex Virus DNA Fragments Located in Epidermal Keratinocytes and Germinative Cells Is Associated with the Development of Erythema Multiforme Lesions

Abstract

Skin from acute and healed herpes simplex virus or herpes simplex virus-associated erythema multiforme (HAEM) lesions was examined by polymerase chain reaction with primers for DNA polymerase, ICP8, thymidine kinase (5' end of herpes simplex virus genome), and ICP27 (3' end of herpes simplex virus genome). The primers were herpes simplex virus specific and equally sensitive. The four herpes simplex virus genes were seen in acute herpes simplex virus lesions, but except for one patient, only polymerase (or polymerase and ICP8) were seen in 7-d healed lesional skin. Herpes simplex virus DNA was not seen 1-1.5 mo after healing. HAEM skins from 18 of 24 patients (75%) were positive for polymerase DNA and four of 24 (17%) were also positive for ICP8 or thymidine kinase DNA. Only one tissue (4%) was positive for polymerase, ICP8, and ICP27 DNA. Skin from healed HAEM lesions was still polymerase DNA positive 1-3 mo after lesion resolution. The polymerase DNA signal was in the basal and spinous cell layers of the epidermis and in the outer root sheath of the hair follicle. Polymerase RNA was identified by reverse transcriptase polymerase chain reaction in skin from acute, but not healed polymerase DNA positive HAEM lesions, suggesting that polymerase expression is associated with HAEM lesion development.

Erythema Multiforme Minor: A Revision

“…The skin from 1-3 months healed HAEM also were PCR positive for the viral Pol gene [32] . In agreement with Imafuku et al [34] the viral DNA is cleared from the skin within 1-1,5 months of HSV lesion resolution, whereas HAEM lesional skin is still positive 1-3 months after healing. Still in agreement with these authors, the positive HSV-DNA was detected in keratinocytes, germinative cells and epithelial cells from the outer root sheath of the hair follicle and in the epithelial cover for sensory nerve endings.…”

“…The Pol RNA was observed in acute but not healed HAEM lesional skin that was positive only for Pol DNA. Therefore, the HAEM lesion development is associated with Pol gene expression [34] . Some others HSV-specific immune mechanisms are involved in the HAEM pathogenesis.…”

CC and CXC Chemokines Are Differentially Expressed in Erythema Multiforme In Vivo

“…24 After linearization of plasmid DNA with appropriate restriction enzymes, 35 Slabeled sense and antisense probes were obtained by in vitro transcription using SP6, T3, or T7 RNA polymerases (Boehringer Ingelheim GmbH, Mannheim, Germany) together with adenosine triphosphate, guanosine triphosphate, cytidine triphosphate (Boehringer Ingelheim GmbH) and [ 35 S]uridine triphosphate (Amersham Biosciences) as substrates. After elimination of the original linearized template cDNA with deoxyribonuclease (Pharmacia LKB Biotechnology, Munich, Germany), alkaline hydrolysis of labeled probes was performed for 30 to 50 minutes.…”

No Evidence of HSV Presence in the Serum of Vitiligo Patients

“…T lymphocytes infiltrating depigmentation spots strongly support that HVT as an environmental factor to stimulate the vitiligo autoimmune response [5]. The distribution pattern of acralfacial vitiligo is similar to erythema multiforme, a condition in a proportion of which there harbored HSV in lesional skin and serum [17]. The most common type of Erythema multiforme is pimples-rash type.…”