Journal
JOURNAL OF VIROLOGY
Volume 81, Issue 11, Pages 6068-6078Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.02743-06
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Funding
- NATIONAL CANCER INSTITUTE [R01CA108951] Funding Source: NIH RePORTER
- NATIONAL CENTER FOR RESEARCH RESOURCES [P20RR015635] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [U54AI057160, T32AI060547, R21AI059132] Funding Source: NIH RePORTER
- NCI NIH HHS [R01CA108951, R01 CA108951] Funding Source: Medline
- NCRR NIH HHS [P20RR15635, P20 RR015635] Funding Source: Medline
- NIAID NIH HHS [U54 AI057160, T32 AI060547, R21 AI059132, R21AI59132] Funding Source: Medline
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The majority of AIDS-associated primary effusion lymphomas (PEL) are latently infected with both Kaposi's sarcoma-associated herpesvirus (KSHV) and Epstein-Barr virus (EBV). PELs harboring two viruses have higher oncogenic potential, suggesting functional interactions between EBV and KSRV. The KSHV replication and transcription activator (K-RTA) is necessary and sufficient for induction of KSHV lytic replication. EBV latent membrane protein 1 (LMP-1) is essential for EBV transformation and establishment of latency in vitro. We show EBV inhibits chemically induced KSHV lytic replication, in part because of a regulatory loop in which K-RTA induces EBV LMP-1 and LMP-1 in turn inhibits K-RTA expression and furthermore the lytic gene expression of KSHV. Suppression of LMP-1 expression in dually infected PEL cells enhances the expression of K-RTA and lytic replication of KSHV upon chemical induction. Because LMP-1 is known to inhibit EBV lytic replication, KSHV-mediated induction of LMP-1 would potentiate EBV latency. Moreover, KSHV infection of EBV latency cells induces LMP-1, and K-RTA is involved in the induction. Both LMP-1 and K-RTA are expressed during primary infection by EBV of KSHV latency cells. Our findings provide evidence that an interaction between EBV and KSRV at molecular levels promotes the maintenance and possibly establishment of viral latency, which may contribute to pathogenesis of PELs.
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