The etiology of atopy is unknown. Its family distribution suggests transmissibility. Populations moving from countries with a low incidence to those with a high incidence increase to the higher rate. African and New Guinea village groups developed asthma with return of individuals who have acquired atopy in the city. Protection (and possibly immunity) develops with early exposure to child care or to affected older siblings. T helper (Th) type 2 clones driving specific allergies remain active even without further allergen exposure. Other IgE responses remain normal. Once boosted to completeness, the patterns of skin test results remain quite stable, possibly by the localization of abnormality maintained by immunity. An example of a virus causing the immortality of Th2 cells is herpes simplex virus type 1. It infects mouse or human Th2 cells and, although it does not multiply, causes immortality by increasing FAS-mediated apoptosis of T cells directed against the infected cells. Human T-cell leukemia virus 1 and probably others use similar ploys. Abnormal levels of FAS receptors and resistance to FAS apoptosis in nasal polyp lymphocytes and abnormal Th2 clones of atopy are interesting in this regard. The localizing role of a staphylococcal superantigen in atopic dermatitis, and possibly in autoimmunity in nonatopic eczema and intrinsic asthma, encourage the consideration of roles for microorganisms in localization and etiology. The epidemiology and characteristics of atopic disease support the plausibility of a viral hypothesis.