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The aim of this study was to determine whether the fingerstick method of obtaining blood is an acceptable alternative to venipuncture for measuring antibody levels. Blood specimens for antibody determination were obtained from healthy adult subjects by venipuncture with the serum separated from the clot by standard methodology. Fingerstick samples were also obtained by piercing the second or third finger and collected in Microtainer serum separator tubes. The serum was then separated by centrifugation, and all specimens were immediately stored at -80 degrees C until assayed. There was an excellent correlation between sera collected from fingerstick and venipuncture for both measles and rubella antibody assays. For the measles enzyme immunoassay (EIA), 85% of subjects were immune, and the correlation coefficient between the fingerstick and the venipuncture results was 0.98 using least squares linear regression. For the rubella EIA, 100% of subjects were immune, and the correlation coefficient was 0.83. Both methods showed the same number of immunopositive individuals; furthermore, there were no cases of immunity to either virus that were detected in only 1 fluid source. There was no significant difference in antibody levels from blood obtained by either method.

Human cytomegalovirus induced beta interferon in cultures of human foreskin cells. The inhibitor was first released between 8 and 16 hours after infection, about 48 hours before progeny virus. In cultures infected with low concentrations of virus, interferon was produced as the infection spread, and then in amounts larger than expected. After infection with cytomegalovirus, cells which had been primed for 48 hours with purified beta interferon produced significantly more interferon than unprimed cells, and the interferon was produced earlier, between 2 and 8 hours after infection. CMV-induced interferon also was able to prime cells. The data suggest that the relatively large quantities of interferon detected in cultures infected with low concentrations of cytomegalovirus result from endogenous priming: those cells infected early first produce interferon which primes uninfected cells, then virus which induces the primed cells to produce interferon in relatively high concentrations.

Human cytomegalovirus disappeared from cultures continuously exposed to interferon. When interferon was removed, high titers of virus reappeared. Cytomegalovirus was thus able to persist in potentially infectious form in cells protected by interferon.