Frohns Florian, Käsmann Anja, Kramer Detlef, Schäfer Britta, Mehmel Mario, Kang Ming, Van Etten James L, Gazzarrini Sabrina, Moroni Anna, Thiel Gerhard
Institute of Botany, Department of Biology, Darmstadt University of Technology, Germany.
J Virol. 2006 Mar;80(5):2437-44. doi: 10.1128/JVI.80.5.2437-2444.2006.
Previous studies have established that chlorella viruses encode K(+) channels with different structural and functional properties. In the current study, we exploit the different sensitivities of these channels to Cs(+) to determine if the membrane depolarization observed during virus infection is caused by the activities of these channels. Infection of Chlorella NC64A with four viruses caused rapid membrane depolarization of similar amplitudes, but with different kinetics. Depolarization was fastest after infection with virus SC-1A (half time [t(1/2)], about 9 min) and slowest with virus NY-2A (t(1/2), about 12 min). Cs(+) inhibited membrane depolarization only in viruses that encode a Cs(+)-sensitive K(+) channel. Collectively, the results indicate that membrane depolarization is an early event in chlorella virus-host interactions and that it is correlated with viral-channel activity. This suggestion was supported by investigations of thin sections of Chlorella cells, which show that channel blockers inhibit virus DNA release into the host cell. Together, the data indicate that the channel is probably packaged in the virion, presumably in its internal membrane. We hypothesize that fusion of the virus internal membrane with the host plasma membrane results in an increase in K(+) conductance and membrane depolarization; this depolarization lowers the energy barrier for DNA release into the host.
先前的研究已经证实，小球藻病毒编码具有不同结构和功能特性的钾离子通道。在本研究中，我们利用这些通道对铯离子的不同敏感性，来确定在病毒感染期间观察到的膜去极化是否由这些通道的活性引起。用四种病毒感染小球藻NC64A会导致类似幅度的快速膜去极化，但动力学不同。感染病毒SC-1A后去极化最快（半衰期[t(1/2)]约为9分钟），而感染病毒NY-2A后最慢（t(1/2)约为12分钟）。铯离子仅在编码对铯离子敏感的钾离子通道的病毒中抑制膜去极化。总体而言，结果表明膜去极化是小球藻病毒与宿主相互作用中的早期事件，并且它与病毒通道活性相关。对小球藻细胞薄片的研究支持了这一观点，这些研究表明通道阻滞剂会抑制病毒DNA释放到宿主细胞中。综合来看，数据表明该通道可能包装在病毒粒子中，大概在其内膜中。我们推测病毒内膜与宿主质膜的融合会导致钾离子电导率增加和膜去极化；这种去极化降低了DNA释放到宿主中的能量屏障。
