Chlorella Viruses Evoke a Rapid Release of K⁺ from Host Cells During the Early Phase of Infection

Authors

• Monika Neupartl, Institute of Botany, Technische Universität Darmstadt, Schnittspahnstrasse 3, D-64287 Darmstadt, Germany
• Christine Meyer, Institute of Botany, Technische Universität Darmstadt, Schnittspahnstrasse 3, D-64287 Darmstadt, Germany
• Isabell Woll, Institute of Botany, Technische Universität Darmstadt, Schnittspahnstrasse 3, D-64287 Darmstadt, Germany
• Florian Frohns, Institute of Botany, Technische Universität Darmstadt, Schnittspahnstrasse 3, D-64287 Darmstadt, Germany
• Ming Kang, University of Nebraska-LincolnFollow
• James L. Van Etten, University of Nebraska-LincolnFollow
• Detlef Kramer, Institute of Botany, Technische Universität Darmstadt, Schnittspahnstrasse 3, D-64287 Darmstadt, Germany
• Brigitte Hertel, Institute of Botany, Technische Universität Darmstadt, Schnittspahnstrasse 3, D-64287 Darmstadt, Germany
• Anna Moroni, Università degli Studi di Milano, Via Celoria 26, 20133 I-Milano, Italy
• Gerhard Thiel, Institute of Botany, Technische Universität Darmstadt, Schnittspahnstrasse 3, D-64287 Darmstadt, GermanyFollow

Document Type

Article

Date of this Version

3-15-2008

Comments

Published in Virology 372:2 (March 15, 2008), pp. 340-348; doi 10.1016/j.virol.2007.10.024 Copyright © 2007 Elsevier Inc. Used by permission. http://www.elsevier.com/locate/yviro

Abstract

Infection of Chlorella NC64A cells by PBCV-1 produces a rapid depolarization of the host probably by incorporation of a viral-encoded K⁺ channel (Kcv) into the host membrane. To examine the effect of an elevated conductance, we monitored the virus-stimulated efflux of K⁺ from the Chlorella cells. The results indicate that all 8 Chlorella viruses tested evoked a host specific K⁺ efflux with a concomitant decrease in the intracellular K⁺. This K⁺ efflux is partially reduced by blockers of the Kcv channel. Qualitatively these results support the hypothesis that depolarization and K⁺ efflux are at least partially mediated by Kcv. The virus-triggered K⁺ efflux occurs in the same time frame as host cell wall degradation and ejection of viral DNA. Therefore, it is reasonable to postulate that loss of K⁺ and associated water fluxes from the host lower the pressure barrier to aid ejection of DNA from the virus particles into the host.