Credit: © 2008 PCCP

Viral attack begins when a virus fuses with a cell membrane. The virus must then prise the membrane open to inject its own genetic material in order to infect the host. Knowing how these events occur, and on what timescales, would enable scientists to develop more effective antiviral drugs that discourage them. Now, Richard Zare and Soonwoo Chah of Stanford University have monitored1 the rupturing processes using surface plasmon resonance (SPR) microscopy, and proposed a mechanism for how a virus ruptures the cell membrane.

They used a simplified model system with an amphipathic helix peptide (AHP) — known to be necessary for the hepatitis C virus to associate with cells — playing the role of the virus. A gold surface was saturated with lipid vesicles — used to mimic cell membranes — while being monitored by SPR microscopy, which can be used dynamically to monitor changes to materials adsorbed on metal surfaces. The SPR signal would be expected to decrease on addition of AHP, the viral mimic, as it attacks and ruptures the vesicles — and this is what was observed, but surprisingly only after a ten-minute induction period.

Zare and Chah propose that the peptides need time to assemble slowly on the surface before initiating their attack. They self-associate on the cell membrane to form oligomers and then reorient, traversing the membrane to form pores. At this point, a virus would be able to inject its genetic material.