To better understand acquired immunity to respiratory-syncytial-virus infections, we analyzed data from a 10-year study of respiratory illness in normal children who were followed longitudinally from early infancy. Immunity was measured in terms of failure to become infected or reduction in severity of clinical illness upon reinfection. Outbreaks of infections occurred seven times over the 10-year-period. During epidemics the attack rate for first infection was 98 per cent. The rate for second infections (75 per cent) was modestly reduced (P less than 0.001); that for third infections was 65 per cent. Age and history of infection both influenced illness. Immunity induced by a single infection had no demonstrable effect on illness associated with reinfection one year later; however, a considerable reduction in severity occurred with the third infection. These observations suggest that amelioration of illness--rather than prevention of infection--may be a realistic goal for immunoprophylaxis.

The mechanisms by which virulent microorganisms mediate host cell injury in respiratory tissue are unclear. To better understand the cellular and subcellular events which accompany these infections requires the establishment of experimental models which permit monitoring of the infectious process under experimentally controlled conditions. During the past several years we have examined the capacity of virulent Mycoplasma pneumoniae organisms, human pathogens of the respiratory tract, to parasitize and produce cell injury in the respiratory epithelium (1-4). Tracheal organ culture served as the highly sensitive host indicator system and its feasibility for other models is recognized (5-9). Based upon our earlier studies we outlined a two step parasitism: (a) the specific attachment of virulent M. pneumoniae via their tip-like organelle to a sialic acid-associated receptor region on the respiratory epithelium and (b) early abnormal host cell function at the transcriptional or translational levels with subsequent tissue cytopathology resulting from the colonization, multiplication, and continued metabolic activity of attached virulent mycoplasmas. The success of this parasitism appeared initially and critically dependent upon the intimate physical association between the membranes ofM. pneumoniae and respiratory epithelial cells. However, the chemical nature of M. pneumoniae surfaces responsible for attachment was unknown.Limited information is available concerning external membrane components of M. pneumoniae. Razin et al. (10,11) extracted from M. pneumoniae a glycolipid which reacts with complement-fixing and metabolic-and growth-inhibiting antibodies raised against intact organisms suggesting a possible surface location of the glycolipid moiety. Additional nonprotein haptens have been demonstrated in other mycoplasma species (12, 13). Boatman and Kenny (14) reported that spherules of M. pneumoniae organisms which form during growth can be disaggregated into individual and viable mycoplasmas by treatment with crude lipase. This observation implied that a lipid moiety on the surface of M. pneumoniae might be responsible for their "stickiness." Other studies with Mycoplasma hominis indicated that membrane proteins exist as receptors for the adsorption of HeLa cells (15) and for indirect hemagglutination activity (16). In this report we examine the unique interaction between virulent M. pneumo-

We analyzed data from a 14-year longitudinal study of respiratory infections in young children to determine the relative importance of viral respiratory infection and nasopharyngeal colonization with Streptococcus pneumoniae and Haemophilus influenzae as factors influencing the occurrence of acute otitis media with effusion. The incidence of this disorder was increased in children with viral respiratory infections (average relative risk, 3.2; P less than 0.0001). Infection with respiratory syncytial virus, influenza virus (type A or B), and adenovirus conferred a greater risk of otitis media than did infection with parainfluenza virus, enterovirus, or rhinovirus. Colonization of the nasopharynx with Str. pneumoniae or H. influenzae had a lesser effect on the incidence of the disease (average relative risk; 1.5; P less than 0.01). Infections with the viruses more closely associated with acute otitis media (respiratory syncytial virus, adenovirus, and influenza A or B) were correlated with an increased risk of recurrent disease. Prevention of selected otitis-associated viral infections should reduce the incidence of this disease.

Attachment of Mycoplasma pneumoniae to host cell by means of a specialized terminus initiates infection. Monoclonal antibodies to a surface protein (Pl) inhibit this process, and react with a region of the tip covered with peplomer-like particles. Since antibodies against the Pl protein are generated by natural and experimental infection and by immunization, the substance may be an important determinant of protective immunity.

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