Abstract
Both neonatal humans and mice are extremely susceptible to lethal HSV infection. In humans there is some evidence for defective anti-HSV antibody production. We have now demonstrated that one week old C57B1/6 mice inoculated i.p. with 104PFU of HSV fail to produce anti-HSV antibody-dependent cellular cytotoxicity (ADCC) antibody prior to death (day 5-7). The ontogeny of antibody production is such that one week old mice produce no antibody, 2 and 3 week old mice produce antibody by day 5, and 4 or 6 week olds by day 3 post infection. Injection of 5×106 adult syngeneic (not allogeneic-Balb/C) peritoneal cells one day prior to HSV infection reconstitutes neonatal antibody production on day 5 (reconstituted 30.7 ± 8.4% ADCC activity, 1/20 dilution versus control 1.1 ± 1.1%, n=6, p < .02) and day 6 (reconstituted 36.7 ± 13.5% versus control 0.3 ± 0.3%, 1/20 dilution, p < .05) and affords survival. Staph protein A absorption and RIA confirm this as IgG antibody. Use of anti-theta or anti-Ia monoclonals plus complement, silica (a macrophage inhibitor), or adherence fractionation has demonstrated the necessity of both adult T cells and macrophages to reconstitute the neonatal antibody production defect. Peritoneal cells thus reconstitute both ADCC effector function and antibody production in neonatal mice. The active or passive reconstitution of human neonates must be investigated. Supported by NIH grant HD13021 and Basic Research Grant 1-914 from the March of Dimes Birth Defects Foundation.
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