Journal
JOURNAL OF VIROLOGY
Volume 82, Issue 9, Pages 4235-4249Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.02370-07
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Funding
- NCI NIH HHS [R01 CA096512, CA124332, CA096512, R01 CA124332] Funding Source: Medline
- NIDCR NIH HHS [DE017333, R01 DE017333] Funding Source: Medline
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Kaposi's sarcoma-associated herpesvirus (KSHV) latency is central to the evasion of host immune surveillances and induction of KSHV-related malignancies. The mechanism of KSHV latency remains unclear. Here, we show that the KSRV latent gene vFLIP promotes viral latency by inhibiting viral lytic replication. vFLIP suppresses the AP-1 pathway, which is essential for KSHV lytic replication, by activating the NF-kappa B pathway. Thus, by manipulating two convergent cellular pathways, vFLIP regulates both cell survival and KSHV lytic replication to promote viral latency. These results also indicate that the effect of the NF-kappa B pathway on KSHV replication is determined by the status of the AP-1 pathway and hence provide a mechanistic explanation for the contradictory role of the NF-kappa B pathway in KSHV replication. Since the NF-kappa B pathway is commonly activated during infection of gammaherpesviruses, these findings might have general implications for the control of gammaherpesviral latency.
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