Cell Membrane-bound Kaposi's Sarcoma-associated Herpesvirus-encoded Glycoprotein B Promotes Virus Latency by Regulating Expression of Cellular Egr-1
| Autor: | Christopher M. Traylen, Shaw M. Akula, Ossie F. Dyson |
|---|---|
| Rok vydání: | 2010 |
| Předmět: |
Gene Expression Regulation
Viral viruses DNA Single-Stranded Viral transformation Biology medicine.disease_cause Biochemistry Virus Viral Envelope Proteins Viral entry Virus latency medicine Humans Kaposi's sarcoma-associated herpesvirus Sarcoma Kaposi Molecular Biology Cells Cultured Cell Membrane Endothelial Cells Molecular Bases of Disease Cell Biology medicine.disease Virology Herpesvirus glycoprotein B Virus Latency Gene Expression Regulation Lytic cycle Viral replication Herpesvirus 8 Human |
| Zdroj: | Journal of Biological Chemistry. 285:37491-37502 |
| ISSN: | 0021-9258 |
| DOI: | 10.1074/jbc.m110.159103 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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