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Human cytomegalovirus (HCMV) infection has been described to impair monocyte differentiation into macrophages and dendritic cells. However, its effect on monocyte-derived osteoclasts is yet to be determined. We showed here that in vitro HCMV infection is associated with an inhibition of osteoclastogenesis through decreased expression of colony stimulating factor 1 receptor (CSF-1R) and RANK in monocytes, which was mediated by an upregulation of quaking I-5 protein (QKI-5), a cellular RNA-interacting protein. We found that deliberate QKI5 overexpression in the absence of HCMV infection is able to decrease CSF-1R and RANK expression, leading to osteoclastogenesis inhibition. Finally, by using lentiviral vectors in a calvarial bone erosion mouse model, we showed that QKI5 inhibits bone degradation. This work identifies QKI5 as a strong inhibitor of bone resorption. Future research will point out whether QKI5 could be a target for bone pathologies. \u00a9 2019 American Society for Bone and Mineral Research.<\/jats:p>\n                  <jats:p>Abstract<\/jats:p>\n                  <jats:p>HCMV infection inhibits osteoclastogenesis through a mechanism involving RNA binding protein QKI5. Overexpression of QKI5 protects from bone degradation and could be a new therapeutic target to limit bone erosion during osteoclast-related diseases.<\/jats:p>","DOI":"10.1002\/jbmr.3943","type":"journal-article","created":{"date-parts":[[2019,12,13]],"date-time":"2019-12-13T14:55:50Z","timestamp":1576248950000},"page":"753-765","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":13,"title":["Inhibition of Osteoclastogenesis by the RNA-Binding Protein QKI5: a Novel Approach to Protect from Bone Resorption"],"prefix":"10.1093","volume":"35","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0826-0299","authenticated-orcid":false,"given":"Benjamin","family":"Rauwel","sequence":"first","affiliation":[{"name":"Centre de Physiopathologie Toulouse Purpan INSERM UMR 1043 Toulouse 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