Neupärtl Monika, Meyer Christine, Woll Isabell, Frohns Florian, Kang Ming, Van Etten James L, Kramer Detlef, Hertel Brigitte, Moroni Anna, Thiel Gerhard
Institute of Botany, Technische Universität Darmstadt, Schnittspahnstrasse 3, D-64287 Darmstadt, Germany.
Virology. 2008 Mar 15;372(2):340-8. doi: 10.1016/j.virol.2007.10.024. Epub 2007 Nov 28.
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.
PBCV-1感染小球藻NC64A细胞可能通过将病毒编码的钾离子通道（Kcv）整合到宿主膜中，从而使宿主细胞迅速去极化。为了研究电导升高的影响，我们监测了病毒刺激下小球藻细胞中钾离子的外流情况。结果表明，所测试的8种小球藻病毒均引发了宿主特异性的钾离子外流，同时细胞内钾离子含量降低。Kcv通道阻滞剂可部分减少这种钾离子外流。从定性角度来看，这些结果支持了去极化和钾离子外流至少部分由Kcv介导的假说。病毒触发的钾离子外流与宿主细胞壁降解以及病毒DNA释放发生在同一时间范围内。因此，合理推测宿主细胞中钾离子的流失及相关水通量的变化会降低压力屏障，有助于病毒颗粒中的DNA释放到宿主细胞中。
