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Journal of Virology, December 1999, p. 10329-10338, Vol. 73, No. 12
Departments of Pediatrics and Microbiology
and Immunology1 and Departments of
Medicine and Cell Biology,2 Vanderbilt
University, Nashville, Tennessee
Received 13 April 1999/Accepted 27 August 1999
Human immunodeficiency virus (HIV) and Kaposi's sarcoma-associated
herpesvirus (KSHV) coinfect many individuals in North America and in
parts of Africa. Infection with HIV is a leading risk factor for the
development of Kaposi's sarcoma (KS). In this study, we tested the
hypothesis that HIV infection of common or adjacent cells would
stimulate replication and spread of KSHV. Infection of a primary
effusion lymphoma cell line by vesicular stomatitis virus type
G-pseudotyped HIV type 1 led to a rapid induction of lytic-phase KSHV
replication. Induction of lytic KSHV replication by HIV required active
replication of HIV. The addition of the nucleoside reverse
transcriptase inhibitor azidothymidine or the protease inhibitor
indinavir to the culture prevented HIV spread and inhibited the
associated induction of KSHV lytic replication. Lytic replication
occurred in both HIV-infected and HIV-uninfected cells within the
culture, and could be induced in uninfected cells via a soluble factor
released from the HIV-infected cells. Transmission of infectious KSHV
to an uninfected target cell was enhanced by HIV replication and was
inhibited by antiretroviral drugs. These results may have implications
for the pathogenesis and treatment of KS in individuals coinfected with
KSHV and HIV.
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
Human Immunodeficiency Virus Replication in a
Primary Effusion Lymphoma Cell Line Stimulates Lytic-Phase Replication
of Kaposi's Sarcoma-Associated Herpesvirus
*
Corresponding author. Mailing address: Vanderbilt
University, Pediatric Infectious Diseases, D-7235 MCN, Nashville, TN
37232-2581. Phone: (615) 322-2250. Fax: (615) 343-9723. E-mail:
paul.spearman{at}mcmail.vanderbilt.edu.
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