Background/Objectives: Viruses are universally found not to have programmed motility functions (propulsion). However, plaque assays of phage 0524phi7-1, an aggregating phage, sometimes generate accelerated bacterial lysis spreading seen via asymmetric, semi-turbid and clear zones in plaque-supporting agarose gels. The semi-turbid zones subsequently clear and expand, without producing phage-resistant bacteria. This apparent phage propulsion could be useful (e.g., for phage therapy of bacterial diseases) if enhanced and better understood. Methods/Results: Here, we found random initiation of semi-turbid zones that were derived from miniature satellite-plaques in numbers too high to reliably count. Previous considerations suggest non-participation of bacterial motors. The known possibilities to explain apparent phage propulsion include diffusiophoresis, driven by concentration gradients between agarose gel fibers, and Marangoni force, derived from surface tension gradients along agarose gel fibers. We found that 1.1% Tween 80, a non-ionic detergent, (1) had no visible effect on either a bacterial lawn or circular plaques, (2) accelerated lysis spreading and (3) drove phage aggregates toward edges of cleared zones, as observed by light microscopy. Electron microscopy demonstrated phage aggregation via lateral tail–tail associations. Conclusions: A working, data-consistent hypothesis is that accelerated lysis spreading is caused by Marangoni force acceleration of monomeric and aggregated phages and phage aggregate exclusion from (previously demonstrated) bacterial clumps.
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Phillips et al. (2026) studied this question.
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