Ion transport blockers inhibit human rhinovirus 2 release

Antiviral Res. 2005 Aug;67(2):98-106. doi: 10.1016/j.antiviral.2005.05.003.


Picornavirus replication causes leakage of cytoplasmic K+ and an influx of Na+ and Ca2+. In this study, we have explored the possibility that a blockade of Ca2+ and Na+ influx would reduce rhinovirus production and/or release. The Ca2+-channel blockers, verapamil and diltiazem, as well as the blocker of Na+/H+ exchange and the epithelial Na+ channel, EIPA, inhibited both virus production and release. The effect on virus release was more pronounced than the effect on production, thus raising the possibility that rhinovirus release may serve as a target for antiviral agents. Unexpectedly, our results also showed that the antiviral activity of the Ca2+-channel blockers was not due to the block of Ca2+ influx. Similarly, the antiviral activity of EIPA appeared to be unrelated to the blockade of cellular Na+/H+ exchanger or the epithelial Na+ channel. Potential alternative mechanisms of the antiviral activity of these compounds are discussed.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Calcium / metabolism
  • Calcium Channel Blockers / pharmacology*
  • Cell Line
  • HeLa Cells
  • Humans
  • Ion Transport / drug effects*
  • Rhinovirus / drug effects*
  • Rhinovirus / physiology


  • Calcium Channel Blockers
  • Calcium