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 journal › Journal article › Research › peer-review
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 language | English |
|---|---|
| Journal | Journal of Virology |
| Volume | 87 |
| Issue number | 7 |
| Pages (from-to) | 4112-7 |
| Number of pages | 6 |
| ISSN | 0022-538X |
| DOIs | |
| Publication status | Published - Apr 2013 |
- 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
Research areas
ID: 48972105