A cellular response protein induced during HSV-1 infection inhibits viral replication by interacting with ATF5Reportar como inadecuado

A cellular response protein induced during HSV-1 infection inhibits viral replication by interacting with ATF5 - Descarga este documento en PDF. Documentación en PDF para descargar gratis. Disponible también para leer online.

Science China Life Sciences

, Volume 56, Issue 12, pp 1124–1133

First Online: 05 December 2013Received: 15 May 2013Accepted: 05 September 2013DOI: 10.1007-s11427-013-4569-y

Cite this article as: Wu, L., Zhang, X., Che, Y. et al. Sci. China Life Sci. 2013 56: 1124. doi:10.1007-s11427-013-4569-y


Studies of herpes simplex virus type 1 HSV-1 infection have shown that many known and unknown cellular molecules involved in viral proliferation are up-regulated following HSV-1 infection. In this study, using two-dimensional polyacrylamide gel electrophoresis, we found that the expression of the HSV-1 infection response repressive protein HIRRP, GI 16552881 was up-regulated in human L02 cells infected with HSV-1. HIRRP, an unknown protein, was initially localized in the cytoplasm and then translocated into the nucleus of HSV-1-infected cells. Further analysis showed that HIRRP represses HSV-1 proliferation by inhibiting transcription of the viral genome by interacting with the cellular transcription factor, ATF5, via its N-terminal domain. ATF5 represses the transcription of many host genes but can also act as an activator of genes containing a specific motif. We found that ATF5 promotes the proliferation of HSV-1 via a potential mechanism by which ATF5 enhances the transcription of viral genes during the course of an HSV-1 infection; HIRRP then induces feedback repression of this transcription by interacting with ATF5.

Keywordsherpes simplex virus type 1 HSV-1 HSV-1 infection response repressive protein HIRPP ATF5 transcriptional regulation This article is published with open access at Springerlink.com

Electronic Supplementary MaterialSupplementary material is available for this article at 10.1007-s11427-013-4569-y and is accessible for authorized users.

Download to read the full article text


Fuente: https://link.springer.com/

Documentos relacionados