The specific cause of Kawasaki disease is unknown. A plausible explanation is that it may be caused by an infection that triggers an inappropriate immunologic cascade in a small number of genetically predisposed children. The pathogenesis is complex and incompletely understood. Various explanations exist. (See #Classification) Circumstantial evidence points to an infectious cause. Since recurrences are unusual in Kawasaki disease, it is thought that the trigger is more likely to be represented by a single pathogen, rather than a range of viral or bacterial agents. Various candidates have been implicated, including upper respiratory tract infection by some novel RNA virus. Despite intensive search, no single pathogen has been identified. There has been debate as to whether the infectious agent might be a superantigen (i.e. one commonly associated with excessive immune system activation). Current consensus favors an excessive immunologic response to a conventional antigen which usually provides future protection. Research points to an unidentified ubiquitous virus, possibly one that enters through the respiratory tract. Seasonal trends in the appearance of new cases of Kawasaki disease have been linked to tropospheric wind patterns, which suggests wind-borne transport of something capable of triggering an immunologic cascade when inhaled by genetically susceptible children. Winds blowing from central Asia correlate with numbers of new cases of Kawasaki disease in Japan, Hawaii, and San Diego. These associations are themselves modulated by seasonal and interannual events in the El Niño–Southern Oscillation in winds and sea surface temperatures over the tropical eastern Pacific Ocean. Efforts have been made to identify a possible pathogen in air-filters flown at altitude above Japan. One source has been suggested in northeastern China. Genetics Genetic susceptibility is suggested by increased incidence among children of Japanese descent around the world, and also among close and extended family members of affected people. Genetic factors are also thought to influence development of coronary artery<unk> s and response to treatment. The exact genetic contribution remains unknown. Genome-wide association studies and studies of individual candidate genes have together helped identify specific single nucleotide polymorphisms (SNPs), mostly found in genes with immune regulatory functions. The associated genes and their levels of expression appear to vary among different ethnic groups, both with Asian and non-Asian backgrounds. SNPs in FCGR2A, CASP3, BLK, ITPKC, CD40 and ORAI1 have all been linked to susceptibility, prognosis, and risk of developing coronary artery<unk> s. Various other possible susceptibility genes have been proposed, including polymorphisms in the HLA region, but their significance is disputed. Genetic susceptibility to Kawasaki disease appears complex. Gene–gene interactions also seem to affect susceptibility and prognosis. At an epigenetic level, altered DNA methylation has been proposed as an early mechanistic factor during the acute phase of the disease.
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