INCREASES IN [CA2-KDA PUTATIVE CELL-MEMBRANE RECEPTOR FOR HCMV GP86(](I) MEDIATED BY THE 92.5)

We determined that changes in intracellular Ca2+ concentration ([Ca2+] (i)) occur in human fibroblasts within the first hour of human cytomeg alovirus (HCMV) infection when viral adsorption and fusion take place, and we investigated whether such changes also occur in response to mo noclonal anti-idiotype antibodies (MAb(2)) that mimic HCMV gp86 and bi nd to a 92.5-kDa putative cell membrane receptor for gp86. Digitized i mage analysis of fura 2-loaded human embryonic lung fibroblasts indica ted specific transient increases in [Ca2+](i) beginning in some cells within the first 5 min of incubation with cross-linked MAb(2) (70-750 nM, P < 0.01), which were similar in timing and intracellular distribu tion to those induced by HCMV. A primary source of Ca2+ appeared to be intracellular Ca2+ stores, since prior depletion of these stores with 30 nM thapsigargin inhibited the response (91.7 +/- 8.6%, P < 0.01); influx of Ca2+ from the extracellular medium was apparently necessary to maintain the intracellular Ca2+ stores. Transient increases in inos itol trisphosphate (IP3) occurred in response to MAb(2) (up to 3,329 /- 84%, P < 0.001) or HCMV (92.8 +/- 19%, P < 0.01) during this same t ime period. These data suggest that the 92.5-kDa receptor for HCMV gp8 6 mediates an increase in IP3 and subsequent release of Ca2+ from intr acellular stores.