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.
Publication types
-
Research Support, N.I.H., Extramural
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Analysis of Variance
-
Animals
-
COS Cells
-
Chlorocebus aethiops
-
Cytomegalovirus / genetics
-
Cytomegalovirus / metabolism
-
Cytomegalovirus / physiology*
-
HEK293 Cells
-
Humans
-
Luciferases
-
Mice
-
Mice, Inbred BALB C
-
Mice, Inbred C57BL
-
Octoxynol
-
Phenotype
-
Receptors, Chemokine / genetics
-
Receptors, Chemokine / metabolism
-
Receptors, G-Protein-Coupled / genetics
-
Receptors, G-Protein-Coupled / metabolism*
-
Salivary Glands / virology*
-
Signal Transduction / genetics
-
Signal Transduction / physiology*
-
Viral Proteins / genetics
-
Viral Proteins / metabolism
-
Viral Tropism / physiology*
-
Virus Activation / physiology*
-
Virus Latency / physiology
Substances
-
Receptors, Chemokine
-
Receptors, G-Protein-Coupled
-
US28 receptor, Cytomegalovirus
-
Viral Proteins
-
seven-transmembrane G-protein-coupled receptor
-
Octoxynol
-
Luciferases