Kaposi's sarcoma-associated herpesvirus sequences in benign lymphoid proliferations not associated with human immunodeficiency virus.

TitleKaposi's sarcoma-associated herpesvirus sequences in benign lymphoid proliferations not associated with human immunodeficiency virus.
Publication TypeJournal Article
Year of Publication1997
AuthorsChadburn A, Cesarman E, Nador RG, Liu YF, Knowles DM
JournalCancer
Volume80
Issue4
Pagination788-97
Date Published1997 Aug 15
ISSN0008-543X
KeywordsAdolescent, Adult, Aged, Aged, 80 and over, Castleman Disease, Child, Child, Preschool, DNA, Viral, Female, Herpesvirus 4, Human, Herpesvirus 8, Human, Humans, Lymph Nodes, Lymphoproliferative Disorders, Male, Middle Aged, Polymerase Chain Reaction, Sequence Analysis, DNA
Abstract

BACKGROUND: Kaposi's sarcoma-associated herpesvirus (KSHV) DNA sequences have been identified in approximately 95% of Kaposi's sarcoma (KS) lesions and primary effusion lymphomas (PELs), suggesting a pathogenetic role for this virus in these lesions. However, KSHV has also been identified in a variety of specimens, including lymph nodes, peripheral blood B cells, semen, and prostate tissue, with varying frequencies. This suggests that KSHV, like Epstein-Barr virus, may be ubiquitously distributed. To evaluate further the clinical spectrum of KSHV infection and define better the prevalence of this virus in lymphoid tissues in the general population, the authors examined a wide spectrum of benign lymphoid proliferations occurring in human immunodeficiency virus (HIV)-negative individuals.

METHODS: One hundred eight lymphoid lesions were examined for the presence of KSHV by polymerase chain reaction (PCR) amplification using primers to open reading frame (ORF) 26. Positive cases were confirmed by Southern blot hybridization using an internal oligonucleotide probe and by PCR amplification using primers to ORF 74 and ORF 75 of the virus.

RESULTS: Only 4 (4%) of 108 specimens were KSHV positive. Three positive lymph node specimens were taken from patients with multicentric Castleman's disease (3 of 11 total cases of Castleman's disease; 3 of 5 total cases of multicentric Castleman's disease). The remaining case was a lymph node showing paracortical hyperplasia, taken from a patient with systemic lupus erythematosus.

CONCLUSIONS: KSHV is not detectable by PCR technology in a wide range of lymphoid proliferations occurring outside of HIV infection. These studies further support the contention that KSHV is preferentially associated with KS, PEL, and some cases of multicentric Castleman's disease.

Alternate JournalCancer
PubMed ID9264363
Grant ListCA68939 / CA / NCI NIH HHS / United States
EY06337 / EY / NEI NIH HHS / United States
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Amy Chadburn, M.D. Ethel Cesarman, M.D., Ph.D.

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