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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-1proliferation 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.
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. Future 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. ATP5 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 du ring the course of an HSV-1 infection; HIRRP then induces feedback repression of this transcription by interacting with ATF5.