title: A cellular response protein induced during HSV-1 infection inhibits viral replication by interacting with ATF5.
abstract: 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.
authors.affiliation: Yunnan Key Laboratory of Vaccine Research & Development on Severe Infectious Diseases, Institute of Medical Biology, Chinese Academy of Medical Sciences & Peking Union Medical College, Kunming, 650118, China.
authors.forename: LianQiu
authors.initials: L
authors.lastname: Wu
authors.forename: XueMei
authors.initials: X
authors.lastname: Zhang
authors.forename: YanChun
authors.initials: Y
authors.lastname: Che
authors.forename: Ying
authors.initials: Y
authors.lastname: Zhang
authors.forename: SongQing
authors.initials: S
authors.lastname: Tang
authors.forename: Yun
authors.initials: Y
authors.lastname: Liao
authors.forename: RuiXiong
authors.initials: R
authors.lastname: Na
authors.forename: Xianglin
authors.initials: X
authors.lastname: Xiong
authors.forename: LongDing
authors.initials: L
authors.lastname: Liu
authors.forename: QiHan
authors.initials: Q
authors.lastname: Li
mesh_terms: D051696:Activating Transcription Factors / Q000737:chemistry / Q000235:genetics / Q000502:physiology; D000818:Animals; D001483:Base Sequence; D002352:Carrier Proteins / Q000737:chemistry / Q000235:genetics / Q000502:physiology*; D002460:Cell Line; D002467:Cell Nucleus / Q000378:metabolism; D002522:Chlorocebus aethiops; D003593:Cytoplasm / Q000378:metabolism; D004279:DNA, Viral / Q000235:genetics / Q000378:metabolism; D015180:Electrophoresis, Gel, Two-Dimensional; D055785:Gene Knockdown Techniques; D016679:Genome, Viral; D057809:HEK293 Cells; D006367:HeLa Cells; D018259:Herpesvirus 1, Human / Q000235:genetics / Q000472:pathogenicity / Q000502:physiology*; D054884:Host-Pathogen Interactions / Q000235:genetics / Q000502:physiology; D006801:Humans; D008969:Molecular Sequence Data; D054730:Protein Interaction Domains and Motifs; D015854:Up-Regulation; D014709:Vero Cells; D014764:Viral Proteins / Q000737:chemistry / Q000235:genetics / Q000502:physiology*; D014779:Virus Replication / Q000235:genetics / Q000502:physiology
chemical_list: C507532:ATF5 protein, human; D051696:Activating Transcription Factors; D002352:Carrier Proteins; D004279:DNA, Viral; C000590718:HSV-1 infection response repressive protein, human; D014764:Viral Proteins