Identification of Herpes Simplex Virus DNA and Lack of Human Herpesvirus-8 DNA in Mycosis Fungoides

Abstract

2a-1 ) 5¢ CTG GTC AGC TTT CGG TAC GA 3¢ , and (HSV Sir, gB 2a-2 ) 5¢ CAG GTC GTG CAG CTG GTT GC 3¢ . These Human herpesvirus 8 ( HHV-8) is the most recent putatprimers have been amplifying both types of HSV, namely types I and II. As a positive control specimen, cerebrospinal ive human herpesvirus. Evidence was obtained using uid of a patient with a clinical and serologically proven HSV molecular biology techniques (1). Speci c DNA encephalitis was used.sequences were rst identi ed in 1994 by Chang et al.(2) in Kaposi's sarcoma tissues from patients with AIDS using the representational diVerence analysis technique.RESULTS AND DISCUSSION In the vast majority of cases, HHV-8 DNA sequences can be shown by polymerase chain reaction (PCR) in Using PCR, we were able to amplify DNA speci c for classical, endemic, iatrogenic and AIDS-associated HSV from 16 of 50 MF patients ( 32%). Thirteen out of Kaposi's sarcoma (1). HHV-8 is also lymphotrophi c 16 HSV-positive samples were diagnosed as MF erythand has the ability to immortalize cells (3, 4). The virus ematous stage and 3 were MF plaque stage. All samples has been associated with peripheral T-cell lymphomas, lacked HHV-8 DNA by PCR. Neither HSV nor HHV-8 plaque parapsoriasis, lymphomatoid papulosis and cutawas detected in any of the control specimens. The neous T-cell lymphomas (CTCL), including mycosis representative positive PCR results are shown in Figs 1 fungoides (MF ) ( 5-7). Herpes simplex virus (HSV ) and 2. primarily targets epithelial and neural cells rather than HHV-8 is usually together with EBV as a dual infeclymphocytes. However, given the immunologic relationtion in body cavity lymphomas, AIDS-related nonship between T lymphocytes and the epidermis, and the Hodgkin's lymphomas and in non-malignant lymphoid fact that MF often appears to be initiated as a cutaneous lesions ( 10, 11 ). In HIV + patients, EBV and HHV-8 process, a potential role for HSV in the development or associated CTCL have been reported to take anaplastic progression of MF has been suggested (8).large cell morphology (12 ). However, there was no The purpose of this study was to elucidate a potential evidence for the presence of EBV (9) and HHV-8 in role for HHV-8 and HSV in the etiopathogenesis of MF.lesional samples of our patients. This nding is in accordance with that of previous studies (5-7, 13-15 ) revealing the absence of HHV-8 in MF and suggesting MATERIAL AND METHODS that HHV-8 can be excluded from the list of potential etiological factors in MF. Fifty formalin-xed paraYn-embedded samples from lesional skin of 50 Caucasian patients with MF were selected and The presence of both HSV-speci c antigens and HSV retrospectively collected from archival les of the Pathology DNA in lesions of CTCL has been reported previously Department. In a previous study performed in our department, (16, 17). However, no direct association between chronic these biopsy samples have been shown by PCR to be EBV HSV infection and the development of malignant negative (9). In all patients, the skin biopsi...

Human herpesvirus 8 is not detectable in lesions of large plaque parapsoriasis, and in early-stage sporadic, familial, and juvenile cases of mycosis fungoides

“…The role of HHV 8 (KSeassociated herpesvirus) in cutaneous lymphoproliferative diseases, including MF and LPP, has been studied in recent years. [8][9][10][11][12][13][14] The genome of HHV 8 contains 86 open reading frames, of which almost 25% encode proteins with either demonstrated or potential immunoregulatory activity. They include homologues of cellular proteins and HHV 8 proteins that can deregulate many aspects of the immune response, including T-and B-cell functions, complement activation, the innate antiviral interferon response, and natural killer cell activity.…”

“…Some authors suggested that viruses may play a role in the development and evolution of MF, either as real oncogenes or as persistent chronic antigens in the skin that induce or maintain T-cell proliferation and activation. 6 The studies performed to date have sought an association of MF with human T-cell lymphotropic type 1 virus 7 ; human herpesviruses (HHV) 6, 7, and 8 [8][9][10][11][12][13][14][15] ; cytomegalovirus 8,16 ; EpsteinBarr virus 8,11,13,17 ; parvovirus 18 ; and polyomavirus SV40. 19 However, evidence of pathogenetic relevance is lacking.…”

“…20 The pathogenetic relevance of HHV 8 in MF and in PPP (mainly large type) has been studied in series from different countries, with contradictory results. [8][9][10][11][12][13][14] The prevalence of HHV 8 varies by geographic region. The rate in the Israeli Jewish population is relatively high, about 11%.…”

High Association of Human Herpesvirus 8 in Large-Plaque Parapsoriasis and Mycosis Fungoides

“…However, initial investigations failed to demonstrate an association. 5,6,20 Moreover, HHV-8 was undetectable in MF lesions of 2 patients with concomitant KS, whereas viral DNA was found in the KS tissue of these patients. 21 In contrast, Trento et al 7 recently reported the detection of HHV-8 infection in skin lesions and peripheral blood of 100% of patients with LPP and in skin lesions and peripheral blood of 25% of patients with MF.…”

Quantificazione mediante PCR dell’EBV-DNA da biopsie cutanee di pazienti con linfomi cutanei primitivi (micosi fungoide e sindrome di Sèzary)

“…L'eziopatogenesi della MF e della SS è ancora ignota e sono stati suggeriti fattori genetici, ambientali ed infettivi (1). Recentemente, il retrovirus HTLVI ed herpesvirus umani sono stati coinvolti sia per la loro potenzialità di trasformazione oncogena diretta, sia perché capaci di infettare le cellule T e stabilire uno stato di latenza nei tessuti dell'ospite (3,4). Il virus di Epstein Barr (EBV), gamma-herpesvirus in grado di infettare in vivo i linfociti B e le cellule epiteliali dell'orofaringe, agente eziologico della mononucleosi infettiva, è notoriamente correlato al carcinoma nasofaringeo ed al linfoma endemico di Burkitt.…”