title: Middle East respiratory syndrome and severe acute respiratory syndrome.
abstract: The recent emergence of the Middle East respiratory syndrome (MERS)-CoV, a close relative of the Severe Acute respiratory syndrome (SARS)-CoV, both of which caused a lethal respiratory infection in humans, reinforces the need for further understanding of coronavirus pathogenesis and the host immune response. These viruses have evolved diverse strategies to evade and block host immune responses, facilitating infection and transmission. Pathogenesis following infection with these viruses is characterized by a marked delay in the induction of Type I interferon (IFN I) and, subsequently, by a poor adaptive immune response. Therapies that expedite IFN I induction as well as interventions that antagonize immunoevasive virus proteins are thus promising candidates for immune modulation.
authors: Interdisciplinary Program in Immunology, University of Iowa, Iowa City, IA 52242, United States.
authors: Rahul
authors: R
authors: Vijay
authors: Interdisciplinary Program in Immunology, University of Iowa, Iowa City, IA 52242, United States; Department of Microbiology, University of Iowa, Iowa City, IA 52242, United States. Electronic address: Stanley-perlman@uiowa.edu.
authors: Stanley
authors: S
authors: Perlman
mesh_terms: D000818:Animals; D018352:Coronavirus Infections / Q000276:immunology* / Q000378:metabolism / Q000635:transmission / Q000821:virology*; D004198:Disease Susceptibility; D000939:Epitopes / Q000276:immunology; D054884:Host-Pathogen Interactions / Q000276:immunology; D006801:Humans; D056747:Immunomodulation; D065207:Middle East Respiratory Syndrome Coronavirus / Q000502:physiology*; D045169:Severe Acute Respiratory Syndrome / Q000276:immunology* / Q000378:metabolism / Q000821:virology*; D016176:T-Lymphocyte Subsets / Q000276:immunology / Q000378:metabolism
chemical_list: D000939:Epitopes