Journal
JOURNAL OF BIOLOGICAL CHEMISTRY
Volume 285, Issue 48, Pages 37491-37502Publisher
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.M110.159103
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Funding
- National Institutes of Health, NIBIB [R21EB006483, 5F31CA132560-02]
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One of the important questions in the field of virus research is about the balance between latent and lytic cycles of replication. Kaposi's sarcoma-associated herpesvirus (KSHV) remains predominantly in a latent state, with only 1-3% of cells supporting a lytic replication at any time. KSHV glycoprotein B (gB) is expressed not only on the virus envelope but also on the surfaces of the few cells supporting lytic replication. Using co-culture experiments, we determined that expression of KSHV gB on as few as 1-2% of human dermal microvascular endothelial cells resulted in a 10-fold inhibition of expression of ORF50, a viral gene critical for the onset of lytic replication. Also, we demonstrate that such a profound inhibitory effect of gB on the lytic cycle of virus replication is by repressing the ability of Egr-1 (early growth response-1) to bind and activate the ORF50 promoter. In general, virus-encoded late stage structural proteins, such as gB, are said to play major roles in virus entry and egress. The present report provides initial evidence supporting a role for membrane-associated gB expressed in a minimal number of cells to promote virus latency. These findings may have ramifications leading to a better understanding of the role of virus-encoded structural proteins not only in KSHV-related diseases but also in other viruses causing latent infections.
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