<p>Parenteral inactivated poliovirus vaccine(IPV) chiefly induces formation of serum antibody. Infection, with oral poliovirus vaccine (OPV) or wild poliovirus, also induces development of secretory IgA antibody. In addition, infection results in virus shedding and, hence, in possible spread of virus to contacts (more likelywith wild than with vaccine virus). IPV induces a high level (90%&ndash;95%) of protection against disease, which presumably is mediated by serum antibody that prevents CNS invasion resulting from viremia. IPV induces little protection against infection but does modify the related virus shedding- chiefly that from the oropharynx. Infection, whether by OPV or wild virus, induces a high level of protection against disease. It also results in appreciable prevention or modification of infection because of the developmentof secretoryIgA antibody. This effect is directly protective for the vaccinee and also benefits the community, since the exposed vaccinee can play little or no part in the spread of wild virus. One major question remaining concerns the maintenance of immunity. Lifelong immunologic memory assures an enhanced serum antibody response to any infection that occurs, but will it be sufficiently rapid that when preinfection antibody cannot be detected newly formed antibody will block blood-borne viral invasion of the CNS? If not, booster doses of vaccineare indicated. OPV boosters might be indicated in any case to reinforce protection against infection and so maintain herd immunity.</p>