this report these data support a kls model in which a ubiquitous infectious agent acquired either through re exposure or reactivation triggers a pathologic th2 response in hiv individuals due to hiv related diminution in th1ifn u03b3 il 2 responses caused by progression of hiv disease fig5 recurrent episodes of kls 5 months to 2 years after resolution of a primary kls episode have been documented in hiv individuals suggesting that reactivation of a latent u201c infection u201d is more likely than re exposure lack of a sentinel lymph node in hiv kls patients may also be a manifestation of a reactivated rather than primary infection referring now to fig5 model of hiv kls a nondescript kd u201c infection u201d occurs in early childhood in the setting of a healthy th1 cellular immune response that controls the infection without development of clinical kawasaki disease in adulthood acquisition of hiv leads to a steady decline in cd4 t cell numbers and a shift toward th2 immune responses after significant degradation of memory t cell immunity the kd agent is able to reactivate unlike the original protective th1 response the secondary response to the kd agent is a less effective th2 response that results in the physical manifestations of kls in general the cytokine milieu in the hiv kls patient with a typical presentation patient 2 was consistent with that previously reported in.