Raf/MEK/ERK signalling triggers reactivation of Kaposi's sarcoma-associated herpesvirus latency
| Autor: | Patrick W. Ford, Benjaman A. Bryan, Shaw M. Akula, Douglas A. Weidner, Vishnu Chintalgattu, Ossie F. Dyson |
|---|---|
| Rok vydání: | 2006 |
| Předmět: |
Proto-Oncogene Proteins B-raf
MAPK/ERK pathway viruses Biology medicine.disease_cause Virus Herpesviridae Cell Line Tumor Virology Phorbol Esters medicine Humans Gammaherpesvirinae Kaposi's sarcoma-associated herpesvirus Extracellular Signal-Regulated MAP Kinases virus diseases Transfection biochemical phenomena metabolism and nutrition biology.organism_classification medicine.disease Lytic cycle Herpesvirus 8 Human Virus Activation Primary effusion lymphoma Mitogen-Activated Protein Kinases Signal Transduction |
| Zdroj: | Journal of General Virology. 87:1139-1144 |
| ISSN: | 1465-2099 0022-1317 |
| DOI: | 10.1099/vir.0.81628-0 |
| Popis: | Kaposi's sarcoma-associated herpesvirus (KSHV) causes Kaposi's sarcoma, primary effusion lymphoma and multicentric Castleman's disease. KSHV infection of cells produces both latent and lytic cycles of infection. In vivo, the virus is found predominantly in the latent state. In vitro, a lytic infection can be induced in KSHV-infected cells by treating with phorbol ester (TPA). However, the exact signalling events that lead to the reactivation of KSHV lytic infection are still elusive. Here, a role is demonstrated for B-Raf/MEK/ERK signalling in TPA-induced reactivation of KSHV latent infection. Inhibiting MEK/ERK signalling by using MEK-specific inhibitors decreased expression of the TPA-induced KSHV lytic-cycle gene ORF8. Transfection of BCBL-1 cells with B-Raf small interfering RNA inhibited TPA-induced KSHV lytic infection significantly. Additionally, overexpression of MEK1 induced a lytic cycle of KSHV infection in BCBL-1 cells. The significance of these findings in understanding the biology of KSHV-associated pathogenesis is discussed. |
| Databáze: | OpenAIRE |
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