title: Human Cytomegalovirus Latency: Approaching the Gordian Knot.
abstract: Herpesviruses have evolved exquisite virus-host interactions that co-opt or evade a number of host pathways to enable the viruses to persist. Persistence of human cytomegalovirus (CMV), the prototypical betaherpesvirus, is particularly complex in the host organism. Depending on host physiology and the cell types infected, CMV persistence comprises latent, chronic, and productive states that may occur concurrently. Viral latency is a central strategy by which herpesviruses ensure their lifelong persistence. Although much remains to be defined about the virus-host interactions important to CMV latency, it is clear that checkpoints composed of viral and cellular factors exist to either maintain a latent state or initiate productive replication in response to host cues. CMV offers a rich platform for defining the virus-host interactions and understanding the host biology important to viral latency. This review describes current understanding of the virus-host interactions that contribute to viral latency and reactivation.
authors: Department of Immunobiology, BIO5 Institute, University of Arizona, Tucson, Arizona 85721; email: fgoodrum@email.arizona.edu.
authors: Felicia
authors: F
authors: Goodrum
mesh_terms: D003587:Cytomegalovirus / Q000235:genetics* / Q000254:growth & development / Q000276:immunology*; D003586:Cytomegalovirus Infections / Q000276:immunology / Q000821:virology; D066246:ErbB Receptors / Q000378:metabolism; D015967:Gene Expression Regulation, Viral / Q000235:genetics; D016679:Genome, Viral / Q000235:genetics; D054884:Host-Pathogen Interactions / Q000235:genetics* / Q000276:immunology; D006801:Humans; D014775:Virus Activation / Q000235:genetics*; D017735:Virus Latency / Q000235:genetics* / Q000276:immunology; D014779:Virus Replication / Q000235:genetics
chemical_list: C512478:EGFR protein, human; D066246:ErbB Receptors
keywords: EGFR; ULb′; cytomegalovirus; herpesvirus; latency; signaling