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

doi:10.1128/JVI.03406-12

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

Eyepath Lab

14 Citations (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.

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	https://doi.org/10.1128/JVI.03406-12
Publication status	Published - Apr 2013

Keywords

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

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Identification of common mechanisms by which human and mouse cytomegalovirus seven-transmembrane receptor homologues contribute to in vivo phenotypes in a mouse model. / Farrell, Helen E; Abraham, Alexander M; Cardin, Rhonda D et al.

In: Journal of Virology, Vol. 87, No. 7, 04.2013, p. 4112-7.

Research output: Contribution to journal › Journal article › Research › peer-review

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

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.",

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author = "Farrell, {Helen E} and Abraham, {Alexander M} and Cardin, {Rhonda D} and Ann-Sofie M{\o}lleskov-Jensen and Rosenkilde, {Mette Marie} and Nicholas Davis-Poynter",

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T1 - Identification of common mechanisms by which human and mouse cytomegalovirus seven-transmembrane receptor homologues contribute to in vivo phenotypes in a mouse model

AU - Farrell, Helen E

AU - Abraham, Alexander M

AU - Cardin, Rhonda D

AU - Mølleskov-Jensen, Ann-Sofie

AU - Rosenkilde, Mette Marie

AU - Davis-Poynter, Nicholas

PY - 2013/4

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N2 - 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.

AB - 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.

KW - Analysis of Variance

KW - Animals

KW - COS Cells

KW - Cercopithecus aethiops

KW - Cytomegalovirus

KW - HEK293 Cells

KW - Humans

KW - Luciferases

KW - Mice

KW - Mice, Inbred BALB C

KW - Mice, Inbred C57BL

KW - Octoxynol

KW - Phenotype

KW - Receptors, Chemokine

KW - Receptors, G-Protein-Coupled

KW - Salivary Glands

KW - Signal Transduction

KW - Viral Proteins

KW - Viral Tropism

KW - Virus Activation

KW - Virus Latency

U2 - 10.1128/JVI.03406-12

DO - 10.1128/JVI.03406-12

M3 - Journal article

C2 - 23345521

SN - 0022-538X

VL - 87

SP - 4112

EP - 4117

JO - Journal of Virology

JF - Journal of Virology

IS - 7

ER -

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

Abstract

Keywords

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