{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,18]],"date-time":"2026-10-18T03:40:29Z","timestamp":1792294829577,"version":"4.4.0"},"reference-count":53,"publisher":"American Society for Microbiology","issue":"1","license":[{"start":{"date-parts":[[2005,1,1]],"date-time":"2005-01-01T00:00:00Z","timestamp":1104537600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["J Virol"],"published-print":{"date-parts":[[2005,1]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            Epstein-Barr virus (EBV) infection is associated with many lymphoproliferative diseases, such as infectious mononucleosis and Burkitt's lymphoma. Consequently, EBV is one of the most extensively studied herpesviruses. Surprisingly, a putative G protein-coupled receptor (GPCR) gene of EBV, BILF1, has hitherto escaped attention, yet BILF1-like genes are conserved among all known lymphocryptovirus species, suggesting that they play a pivotal role in viral infection. To determine the function of EBV BILF1, the activity of this gene and its products was studied. BILF1-specific mRNA was detected in various EBV-positive cell types and found to be expressed predominantly during the immediate early and early phases of infection in vitro. Interestingly, in COS-7 cells transfected with BILF1 expression constructs, a decrease in forskolin-induced CRE-mediated transcription was measured, as well as an increase in NF-\u03baB-mediated transcription. In contrast, CRE-mediated transcription was increased in EBV-positive Burkitt's lymphoma cells as well as EBV-positive lymphoblastoid B cells transfected with BILF1, whereas NF-\u03baB-mediated transcription levels remained unaffected in these cells. All observed activities were sensitive to treatment with pertussis toxin, indicating that the BILF1-encoded protein mediates these activities by coupling to G proteins of the G\n            <jats:sub>i\/o<\/jats:sub>\n            class. Finally, reduced levels of phosphorylated RNA-dependent antiviral protein kinase were observed in COS-7 and Burkitt's lymphoma cells transfected with BILF1. Neither of the observed effects required a ligand to interact with the BILF1 gene product, suggesting that BILF1 encodes a constitutively active GPCR capable of modulating various intracellular signaling pathways.\n          <\/jats:p>","DOI":"10.1128\/jvi.79.1.441-449.2005","type":"journal-article","created":{"date-parts":[[2004,12,16]],"date-time":"2004-12-16T03:52:43Z","timestamp":1103169163000},"page":"441-449","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":97,"title":["The Epstein-Barr Virus BILF1 Gene Encodes a G Protein-Coupled Receptor That Inhibits Phosphorylation of RNA-Dependent Protein Kinase"],"prefix":"10.1128","volume":"79","author":[{"given":"Patrick S.","family":"Beisser","sequence":"first","affiliation":[{"name":"Department of Medical Microbiology, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dennis","family":"Verzijl","sequence":"additional","affiliation":[{"name":"Division of Medicinal Chemistry, Leiden\/Amsterdam Center for Drug Research, Free University, Amsterdam, The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yvonne K.","family":"Gruijthuijsen","sequence":"additional","affiliation":[{"name":"Department of Medical Microbiology, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Erik","family":"Beuken","sequence":"additional","affiliation":[{"name":"Department of Medical Microbiology, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Martine J.","family":"Smit","sequence":"additional","affiliation":[{"name":"Division of Medicinal Chemistry, Leiden\/Amsterdam Center for Drug Research, Free University, Amsterdam, The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rob","family":"Leurs","sequence":"additional","affiliation":[{"name":"Division of Medicinal Chemistry, Leiden\/Amsterdam Center for Drug Research, Free University, Amsterdam, The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cathrien A.","family":"Bruggeman","sequence":"additional","affiliation":[{"name":"Department of Medical Microbiology, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cornelis","family":"Vink","sequence":"additional","affiliation":[{"name":"Department of Medical Microbiology, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1038\/385347a0"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1038\/310207a0"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1038\/34193"},{"key":"e_1_3_2_5_2","unstructured":"Becker Y. 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