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Blood, Vol. 93 No. 12 (June 15), 1999:
pp. 4044-4058
Reactivation and Persistence of Human Herpesvirus-8 Infection in B
Cells and Monocytes by Th-1 Cytokines Increased in Kaposi's
Sarcoma
Paolo Monini,
Sandra Colombini,
Michael Stürzl,
Delia Goletti,
Aurelio Cafaro,
Cecilia Sgadari,
Stefano Buttò,
Marina Franco,
Patrizia Leone,
Stefano Fais,
Pasqualina Leone,
Gianna Melucci-Vigo,
Chiara Chiozzini,
Francesca Carlini,
Gudrun Ascherl,
Emmanuelle Cornali,
Christian Zietz,
Eric Ramazzotti,
Fabrizio Ensoli,
Massimo Andreoni,
Patrizio Pezzotti,
Giovanni Rezza,
Robert Yarchoan,
Robert C. Gallo, and
Barbara Ensoli
From the Laboratory of Virology, Istituto Superiore di Sanità,
Rome, Italy; the Institute of Human Virology, University of Maryland at
Baltimore, Baltimore, MD; GSF-National Research Center for Environment
and Health, Institute of Molecular Virology, Neuherberg, Germany;
Max-Planck-Institut für Biochemie, Abteilung für
Virusforschung, Martinsried, Germany; Pathologisches Institut der
LMU-München, München, Germany; the Department of Allergy
and Clinical Immunology, University of Rome "La Sapienza," Rome,
Italy; the Chair of Infectious Disease, University of "Tor
Vergata," Rome Italy; the Laboratory of Epidemiology and
Biostatistics, Istituto Superiore di Sanità, Rome, Italy; and the
HIV and AIDS Malignancy Branch, National Cancer Institute, National
Institutes of Health, Bethesda, MD.
Patients with Kaposi's sarcoma (KS) have a human herpesvirus-8
(HHV-8) load higher than patients without KS and present a CD8+ T-cell activation with production of Th1-type
cytokines both in tissues and peripheral blood mononuclear cells
(PBMC). Because in tissues of KS patients detection of inflammatory
cytokines (IC) can precede detection of HHV-8 DNA and because signs of
immunoactivation and/or dysregulation can precede KS development, we
investigated the effect of IC on HHV-8 infection. To achieve this goal,
PBMC and purified cell populations from 45 patients with KS and 45 patients at risk of KS were analyzed for HHV-8 DNA and/or gene expression and for cell survival, growth, and phenotype before or after
culture with or without the IC increased in KS. The results indicate
that PBMC that are polymerase chain reaction (PCR)-positive at day 0 generally loose the virus upon culture. However, the presence of IC
maintains HHV-8 DNA load in cultured cells. In addition, IC increase
viral load to detectable levels in PBMC from serologically positive
patients that were PCR-negative before culture.  Interferon is
sufficient for these effects, whereas tumor necrosis factor and
interleukin-6 have little or no activity. The increase of HHV-8 DNA by
IC is observed after short-term (7 days) or long-term (28 days) culture
of the cells and occurs in one or both of the two circulating cell
types that are infected in vivo: B cells and monocytes. In both cases
it is associated with lytic gene expression, suggesting that virus
reactivation is one of the most likely mechanisms for the effect of IC
on virus load. However, IC have also effects on the cells target of
HHV-8 infection, because they increase B-cell survival and induce the growth and differentiation of monocytes into KS-like spindle cells with
markers of endothelial macrophages. Because cells with markers of
endothelial macrophages are present in blood and lesions from KS
patients and are infected by HHV-8, these data may explain the high
HHV-8 load associated with KS development and suggest that infected
monocytes may carry the virus to tissues, transmit the infection, or
differentiate in loco in spindle cells with endothelial macrophage markers.
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