Pneumococcal surface protein A (PspA), pneumococcal surface adhesin A (PsaA), and pneumolysin (Ply) are common to virtually all Streptococcus pneumoniae isolates. They are immunogenic and protective against pneumococcal challenge in animals and are the major candidates for a protein-based pneumococcal vaccine for humans. However, little is known of the natural development of antibodies to these proteins in humans. The objective of this study was to evaluate the natural development of antibodies to PspA, PsaA, and Ply in relation to pneumococcal infection and carriage in young children. Serum antibodies to these proteins were measured by EIA in children at ages 6, 12, 18, and 24 months and in their mothers. All age groups were capable of producing antibodies to the 3 proteins. The antibody concentrations increased with age and were strongly associated with pneumococcal exposure, whether by carriage or infection (acute otitis media).

SUMMARYThe contribution of serotype-speci®c IgG concentration, subclasses, and avidity to opsonophagocytic activity (OPA) against Streptococcus pneumoniae (Pnc) was evaluated in sera of adults and infants immunized with different pneumococcal vaccines. Antibody concentrations and avidities were measured by enzymeimmunoassay (EIA) and OPAs by killing assay of Pnc. The most important factor contributing positively to OPA was the speci®c IgG level. In infants, a tendency to negative correlation was found between the concentration needed for killing of bacteria and avidity, suggesting that less antibodies of high rather than low avidity were required for killing. No such correlation was seen in adults. However, in adults the avidity was high already before vaccination and the variation was narrow. Thus, avidity was probably not a limiting factor in¯uencing OPA. The effect of IgG2/IgG1 ratio on OPA was mostly negative but insigni®cant.

PncCRM induces both systemic and mucosal immune responses in infants.

Differences between Finland and Sardinia in the seasonal pattern for the incidence of newly diagnosed IDDM cannot be explained by differences in climate, temperature, a longer warm period in Sardinia, or other climatic phenomena. The results do not provide evidence in favor of a specific viral etiology of IDDM. It may be suggested that there are triggering events at certain times, but they are likely to be unspecific. Nevertheless, why the incidence of IDDM in these two populations is equally high despite differences in climate, environment, and genetic background remains an unsolved question.

Lowered IFN responses in children suffering from recurrent URIs and/or AOM may, in a subgroup of the children, be due to a genetic property of the child. However, because of the great interindividual variations, we cannot use the IFN production capacity as such for prediction of forthcoming respiratory infections and/or otitis media.

The systematic search of aetiological agents from a variety of slowly progressing or subacute neurological diseases has revealed causative viruses or virus-like agents from kuru, Creutzfeldt-Jacob disease and other forms of presenile dementias, subacute sclerosing panencephalitis, progressive multifocal encephalopathy, and from many similar neurological diseases in animals (Gajdusek and Gibbs, 1973; Gajdusek, 1973). The first two diseases called subacute spongiform virus encephalopathies (Gajdusek and Gibbs, 1971) have many interesting features including heredo-familial occurrence and totally non-inflammatory neuropathology. Thus the epidemiology of these diseases is not typical for diseases with infectious aetiology, and the histopathological studies do not suggest the presence of extremely high-titred infectious material in brain cells.

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