title: Modulation of host innate and adaptive immune defenses by cytomegalovirus: timing is everything.
abstract: Human cytomegalovirus (HCMV) (HHV-5, a beta-herpesvirus) causes the vast majority of infection-related congenital birth defects, and can trigger severe disease in immune suppressed individuals. The high prevalence of societal infection, the establishment of lifelong persistence and the growing number of immune-related diseases where HCMV is touted as a potential promoter is slowly heightening public awareness to this virus. The millions of years of co-evolution between CMV and the immune system of its host provides for a unique opportunity to study immune defense strategies, and pathogen counterstrategies. Dissecting the timing of the cellular and molecular processes that regulate innate and adaptive immunity to this persistent virus has revealed a complex defense network that is shaped by CMV immune modulation, resulting in a finely tuned host-pathogen relationship.
authors.affiliation: Division of Molecular Immunology, La Jolla Institute for Allergy and Immunology, La Jolla, CA, USA.
authors.forename: A
authors.initials: A
authors.lastname: Loewendorf
authors.forename: C A
authors.initials: CA
authors.lastname: Benedict
mesh_terms: D000818:Animals; D003587:Cytomegalovirus / Q000276:immunology*; D003586:Cytomegalovirus Infections / Q000276:immunology* / Q000635:transmission; D006801:Humans; D007107:Immune System / Q000276:immunology*; D007111:Immunity, Cellular; D007372:Interferons / Q000276:immunology; D051379:Mice; D016328:NF-kappa B / Q000276:immunology; D013154:Spleen / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology; D013997:Time Factors; D019562:Viral Load
chemical_list: D016328:NF-kappa B; D007372:Interferons