Abstract
The human cytomegalovirus (CMV) proteins US28 and UL33 are homologous to chemokine receptors (CKRs). Knockout of the mouse CMV M33 protein (UL33 homologue) results in substantial attenuation of salivary gland infection/replication and reduced efficiency of reactivation from tissue explants. M33-mediated G protein-coupled signaling is critical for the salivary gland phenotype. In this report, we demonstrate that US28 and (to a lesser degree) UL33 restore reactivation from tissue explants and partially restore replication in salivary glands (compared to a signaling-deficient M33 mutant). These studies provide a novel small animal model for evaluation of therapies targeting the human CMV CKRs.
Original language | English |
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Journal | Journal of Virology |
Volume | 85 |
Issue number | 12 |
Pages (from-to) | 6091-5 |
Number of pages | 5 |
ISSN | 0022-538X |
DOIs | |
Publication status | Published - Jun 2011 |
Keywords
- Animals
- Cytomegalovirus
- Cytomegalovirus Infections
- Disease Models, Animal
- Female
- Herpesviridae Infections
- Humans
- Mice
- Mice, Inbred BALB C
- Muromegalovirus
- Organ Specificity
- Receptors, Chemokine
- Salivary Glands
- Viral Proteins
- Virus Activation
- Virus Latency
- Virus Replication