The following findings were made from observations of adenovirus (AV) infections in Seattle VW families, 1965-1969, which extended the 1961-1965 New York VW studies: That infections are predominantly enteric, may be abortive or invasive and followed by persistent intermittent excretion was confirmed. That such excretion is most characteristic of types 1, 2, 3 and 5 viruses may explain why these types were usually endemic. However, since observed duration of excretion was not increased despite a longer average observation period, persistent excretion appears not to continue indefinitely and generation-to-generation transmission now seems improbable. Unilike New York, alternate cycling of types 1 and 2 viruses was not seen. Among homotypic susceptibles, infection rates for the endemic types were highest in infants (greater than 90% for types 1 and 2), decreased with age in older children but increased in parents, perhaps because of closer contact with infants. Development of serum neutralizing antibody was most frequent (about 90%) after types 1 and 2 infection; in all cases, titers decayed over time. While delayed virus spread related to persistent intermittent excretion did occur, spread closely following new or renewed (after larger than or equal to 3 months) excretion was more important. Sibling introducers were more effective spreaders than infants, and duration of excretion was more important than mode. These data indicate that homotypic immunity is 85% protective against infection. A protective effect of heterotypic immunity could not be shown. Illness (chiefly respiratory and often febrile) was associated with 49% of infections in susceptibles and with 65% when respiratory shedding occurred. The contribution of AV to all infectious illness, based on virus-positive infections only, was 5% in infants and 3% in the 2-4-year age group; for febrile illness, the corresponding contributions were about 10% and 5%. Inclusion of infections discovered only be serology (49% of all infections) would greatly increase the contribution of AV to illness.