Presented in part at the 1996 meeting of the United States and Canadian Academy of Pathology, Washington, DC.
Kaposi's sarcoma-associated herpesvirus sequences in benign lymphoid proliferations not associated with human immunodeficiency virus†
Version of Record online: 20 NOV 2000
Copyright © 1997 American Cancer Society
Volume 80, Issue 4, pages 788–797, 15 August 1997
How to Cite
Chadburn, A., Cesarman, E., Nador, R. G., Liu, Y. F. and Knowles, D. M. (1997), Kaposi's sarcoma-associated herpesvirus sequences in benign lymphoid proliferations not associated with human immunodeficiency virus. Cancer, 80: 788–797. doi: 10.1002/(SICI)1097-0142(19970815)80:4<788::AID-CNCR18>3.0.CO;2-P
- Issue online: 20 NOV 2000
- Version of Record online: 20 NOV 2000
- Manuscript Revised: 4 APR 1997
- Manuscript Accepted: 4 APR 1997
- Manuscript Received: 12 DEC 1996
- National Institutes of Health awarded to(D.M.K. & E.C.). Grant Numbers: EY06337, CA68939
- Kaposi's sarcoma-associated herpesvirus;
- human herpesvirus-8;
- Castleman's disease
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.
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.
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.
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. Cancer 1997; 80:788-97. © 1997 American Cancer Society.