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Myeloid differentiation coupled with immune dysregulation leads to viral reactivation, which can cause severe disease and mortality. Reactivation of latent virus requires chromatin reorganization and the removal of transcriptional repressors in exchange for transcriptional activators. While some factors involved in these processes are identified, a complete characterization of the viral and cellular factors involved in their upstream regulation remains elusive. Herein we show the HCMV-encoded G protein-coupled receptor (GPCR), UL33, is expressed during latency. While this viral GPCR is not required to maintain latent infection, our data reveal UL33-mediated signaling is important for efficient viral reactivation. Additionally, UL33 signaling induces cellular cAMP response element binding protein (CREB) phosphorylation, a transcription factor whose recruitment to the major immediate early (MIE) enhancer\/promoter promotes reactivation. Finally, targeted pharmacological inhibition of CREB activity reverses the reactivation phenotype of the UL33 signaling deficient mutant. In sum, our data reveal UL33-mediated signaling functions to activate CREB, resulting in successful viral reactivation.<\/jats:p>","DOI":"10.1242\/jcs.254268","type":"journal-article","created":{"date-parts":[[2020,11,16]],"date-time":"2020-11-16T15:05:56Z","timestamp":1605539156000},"source":"Crossref","is-referenced-by-count":21,"title":["CMV-encoded GPCR pUL33 activates CREB and facilitates its recruitment to the MIE locus for efficient viral reactivation"],"prefix":"10.1242","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0919-2961","authenticated-orcid":false,"given":"Benjamin A.","family":"Krishna","sequence":"first","affiliation":[{"name":"Genomic Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7712-6259","authenticated-orcid":false,"given":"Amanda B.","family":"Wass","sequence":"additional","affiliation":[{"name":"Genomic Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5106-1722","authenticated-orcid":false,"given":"Abigail L.","family":"Dooley","sequence":"additional","affiliation":[{"name":"Genomic Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christine M.","family":"O'Connor","sequence":"additional","affiliation":[{"name":"Genomic Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"237","published-online":{"date-parts":[[2020,1,1]]},"reference":[{"key":"2021042623320772000_JCS254268C1","doi-asserted-by":"publisher","first-page":"110","DOI":"10.3390\/v12010110","article-title":"Bright and early: inhibiting human cytomegalovirus by targeting major immediate-early gene expression or protein function","volume":"12","author":"Adamson","year":"2020","journal-title":"Viruses"},{"key":"2021042623320772000_JCS254268C2","doi-asserted-by":"publisher","first-page":"8855","DOI":"10.1128\/JVI.00741-16","article-title":"Multiple transcripts encode full-length human cytomegalovirus IE1 and IE2 proteins during lytic infection","volume":"90","author":"Arend","year":"2016","journal-title":"J. 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