Abstract
Analysis of a genome-scale RNA interference screen of host factors affecting herpes simplex virus type 1 (HSV-1) revealed that the mineralocorticoid receptor (MR) inhibits HSV-1 replication. As a ligand-activated transcription factor the MR regulates sodium transport and blood pressure in the kidney in response to aldosterone, but roles have recently been elucidated for the MR in other cellular processes. Here, we show that the MR and other members of the mineralocorticoid signalling pathway including HSP90 and FKBP4, possess anti-viral activity against HSV-1 independent of their effect on sodium transport, as shown by sodium channel inhibitors. Expression of the MR is upregulated upon infection in an interferon (IFN) and viral transcriptional activator VP16-dependent fashion. Furthermore, the MR and VP16, together with the cellular co-activator Oct-1, transactivate the hormone response element (HRE) present in the MR promoter and those of its transcriptional targets. As the MR induces IFN expression, our data suggests the MR is involved in a positive feedback loop that controls HSV-1 infection.
Item Type: | Journal article |
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Faculties: | Mathematics, Computer Science and Statistics > Computer Science |
Subjects: | 500 Science > 570 Life sciences; biology 600 Technology > 600 Technology |
URN: | urn:nbn:de:bvb:19-epub-59447-1 |
ISSN: | 2045-2322 |
Language: | English |
Item ID: | 59447 |
Date Deposited: | 05. Dec 2018, 08:42 |
Last Modified: | 13. Aug 2024, 12:56 |