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Detection of Human Herpesvirus 8 in Korean Kaposi's Sarcoma Cases by Polymerase Chain Reaction and In situ Polymerase Chain Reaction
Author(s) -
Jang HoSun,
Park JungHum,
Oh ChangKeun,
Kwon KyungSool
Publication year - 1999
Publication title -
the journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.9
H-Index - 65
eISSN - 1346-8138
pISSN - 0385-2407
DOI - 10.1111/j.1346-8138.1999.tb02022.x
Subject(s) - polymerase chain reaction , nested polymerase chain reaction , virology , biology , sarcoma , virus , human herpesvirus , in situ , human herpesvirus 6 , microbiology and biotechnology , pathology , herpesviridae , viral disease , medicine , gene , chemistry , genetics , organic chemistry
Several infectious agents, including herpesvirus‐like particles, had been suggested as possible candidates for the development of Kaposi's sarcoma (KS), and a new herpesvirus, human herpesvirus 8 (HHV‐8), was recently identified in the vast majority of KS lesions, irrespective of their association with human immunodeficiency virus (HIV) infection. However, the etiologic role of HHV‐8 in KS remains controversial. We undertook this study to screen for and localize the presence of HHV‐8 in KS in Korea. A total of 46 paraffin‐embedded specimens were studied, including KS, hemangioproliferative disorders, and 10 non‐KS lesions from HIV‐positive patients. We performed nested polymerase chain reaction (PCR) and in situ PCR with HHV‐8 specific primers. HHV‐8 DNA sequences were detected in 8 of 11 KS specimens. All specimens of hemangioproliferative disorders, non‐KS lesions from HIV‐positive patients, and other skin samples were negative for HHV‐8. When sequencing PCR products, the sequences were almost identical with the prototypic sequence for HHV‐8. In PCR‐positive tissues, in situ PCR staining of HHV‐8 localized to nuclei of endothelial cells and perivascular spindle‐shaped tumor cells. The results of this study suggest that HHV‐8 is not widespread and has a certain causative role in the development of KS. Further studies, including serological and animal studies, will be helpful to appreciate an epidermiological link and pathogenetic mechanism between HHV‐8 and KS.