Identification of common mechanisms by which human and mouse cytomegalovirus seven-transmembrane receptor homologues contribute to in vivo phenotypes in a mouse model

Helen E Farrell, Alexander M Abraham, Rhonda D Cardin, Ann-Sofie Mølleskov-Jensen, Mette Marie Rosenkilde, Nicholas Davis-Poynter

14 Citationer (Scopus)

Abstract

The mouse cytomegalovirus chemokine receptor homologue (CKR) M33 is required for salivary gland tropism and efficient reactivation from latency, phenotypes partially rescued by the human cytomegalovirus CKR US28. Herein, we demonstrate that complementation of salivary gland tropism is mediated predominantly by G protein-dependent signaling conserved with that of M33; in contrast, both G protein-dependent and -independent pathways contribute to the latency phenotypes. A novel M33-dependent replication phenotype in cultured bone marrow macrophages is also described.
OriginalsprogEngelsk
TidsskriftJournal of Virology
Vol/bind87
Udgave nummer7
Sider (fra-til)4112-7
Antal sider6
ISSN0022-538X
DOI
StatusUdgivet - apr. 2013

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