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Increases in [Ca2+]i mediated by the 92.5-kDa putative cell membrane receptor for HCMV gp86

S Keay1, B R Baldwin, M W Smith

  • 1Department of Medicine, University of Maryland School of Medicine, Baltimore, USA.

The American Journal of Physiology
|July 1, 1995
PubMed

Insights

Human cytomegalovirus (HCMV) infection triggers intracellular calcium ([Ca2+]i) changes. Mimicking antibodies also induce these calcium shifts, suggesting a specific receptor mediates this response.

Area of Science:

  • Cellular Biology
  • Virology
  • Immunology

Background:

  • Human cytomegalovirus (HCMV) infection is known to alter intracellular calcium levels ([Ca2+]i) during early infection stages.
  • A 92.5-kDa cell membrane receptor for HCMV gp86 has been identified.

Purpose of the Study:

  • To investigate if monoclonal anti-idiotype antibodies (MAb2), mimicking HCMV gp86, can induce intracellular calcium changes similar to HCMV infection.
  • To explore the role of the putative 92.5-kDa receptor in mediating these calcium responses.

Main Methods:

  • Digitized image analysis of fura 2-loaded human embryonic lung fibroblasts.
  • Treatment with cross-linked MAb2 and HCMV.
  • Depletion of intracellular calcium stores using thapsigargin.
  • Measurement of inositol trisphosphate (IP3) levels.

Main Results:

  • Cross-linked MAb2 induced transient increases in [Ca2+]i within 5 minutes, mirroring HCMV infection.
  • The calcium response was primarily sourced from intracellular stores, as indicated by inhibition after thapsigargin treatment.
  • Both MAb2 and HCMV induced transient increases in inositol trisphosphate (IP3).

Conclusions:

  • The 92.5-kDa receptor for HCMV gp86 appears to mediate an increase in IP3.
  • This IP3 increase subsequently triggers the release of calcium from intracellular stores.
  • These findings elucidate an early molecular mechanism of HCMV infection involving calcium signaling.

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