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

Research output: Contribution to journalJournal articleResearchpeer-review

  • Helen E Farrell
  • Alexander M Abraham
  • Rhonda D Cardin
  • Ann-Sofie Mølleskov-Jensen
  • Rosenkilde, Mette
  • Nicholas Davis-Poynter
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.
Original languageEnglish
JournalJournal of Virology
Issue number7
Pages (from-to)4112-7
Number of pages6
Publication statusPublished - Apr 2013

    Research areas

  • Analysis of Variance, Animals, COS Cells, Cercopithecus aethiops, Cytomegalovirus, HEK293 Cells, Humans, Luciferases, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Octoxynol, Phenotype, Receptors, Chemokine, Receptors, G-Protein-Coupled, Salivary Glands, Signal Transduction, Viral Proteins, Viral Tropism, Virus Activation, Virus Latency

ID: 48972105