Infectious diseases and immunizationNew developments in the search for the etiologic agent of Kawasaki diseaseRowley, Anne H; Shulman, Stanford T Author Information Northwestern University Feinberg School of Medicine, The Children's Memorial Hospital, Chicago, Illinois, USA Correspondence to Anne H. Rowley, MD, Northwestern University Feinberg School of Medicine, Pediatrics W140, Ward 12-204, 303 E Chicago Avenue, Chicago, IL 60611, USA Fax: +1 312 503 1181; e-mail: [email protected] Current Opinion in Pediatrics: February 2007 - Volume 19 - Issue 1 - p 71-74 doi: 10.1097/MOP.0b013e328012720f Buy Metrics Abstract Purpose of review The aim of this article is to review recent developments in the search for the etiologic agent of Kawasaki disease. Recent findings Two recently proposed theories of Kawasaki disease etiology, the toxic shock syndrome toxin-1 hypothesis and the coronavirus NL-63 hypothesis, have been studied extensively and have been disproven. Surprisingly, IgA plasma cells infiltrate inflamed tissues in acute Kawasaki disease, including the coronary artery, and are oligoclonal, or antigen-driven. Synthetic versions of predominant IgA antibodies in acute Kawasaki disease arterial tissue bind to an antigen present in acute Kawasaki disease ciliated bronchial epithelium and in a subset of macrophages in acute inflamed Kawasaki disease tissues. Light and electron microscopic studies of the antigen in acute Kawasaki disease ciliated bronchial epithelium indicate that the Kawasaki disease-associated antigen localizes to cytoplasmic inclusion bodies that are consistent with aggregates of viral protein and associated nucleic acid. Summary The identification of cytoplasmic inclusion bodies in acute Kawasaki disease ciliated bronchial epithelium has provided direction for future Kawasaki disease etiology studies. Transmission electron microscopic examination of glutaraldehyde-fixed medium-sized bronchi from acute Kawasaki disease fatalities and analysis of the protein and nucleic acid components of the inclusions should provide important information about these inclusion bodies and speed the identification of the specific etiologic agent of Kawasaki disease. © 2007 Lippincott Williams & Wilkins, Inc.