Poliovirus type I LSc strain labeled with '4C-uridine was adsorbed onto isolated plasma membranes and incubated with them. When membranes from Hep-2 or Vero cells were used, 22% of the label was converted to a trichloroacetic acid-soluble form, when trypsin or ribonuclease was added, the fraction rendered soluble was increased, and when the two enzymes were added in sequence, 85% or more of the label became trichloroacetic acid-soluble. This labilization of poliovirus could be reproduced when butanol-solubilized proteins from membranes were substituted for the whole plasma membranes, but it did not occur with membranes from poliovirus-resistant calf kidney or BHK-21 cells.

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The pathogenesis of rheumatic fever has been linked to various immune mechanisms involving streptococcal antibodies and heart tissue antigens. Latent myocarditis due to group B coxsackievirus has also been considered as a possible conditioning factor. The validity of the role of infection with group B coxsackievirus in rheumatic fever was tested by determining the incidence of type-specific neutralizing antibodies in sera of Filipino children. Analysis of the results by means of a normal Z-test showed that the incidence in rheumatic children was not statistically significant in comparison to the incidence in asymptomatic children.