Abstract

How viruses are transmitted across the mucosal epithelia of the respiratory, digestive, or excretory tracts, and how they spread from cell to cell and cause systemic infections, is incompletely understood. Recent advances from single virus tracking experiments have revealed conserved patterns of virus movements on the plasma membrane, including diffusive motions, drifting motions depending on retrograde flow of actin filaments or actin tail formation by polymerization, and confinement to submicrometer areas. Here, we discuss how viruses take advantage of cellular mechanisms that normally drive the movements of proteins and lipids on the cell surface. A concept emerges where short periods of fast diffusive motions allow viruses to rapidly move over several micrometers. Coupling to actin flow supports directional transport of virus particles during entry and cell-cell transmission, and local confinement coincides with either nonproductive stalling or infectious endocytic uptake. These conserved features of virus–host interactions upstream of infectious entry offer new perspectives for anti-viral interference.

Highlights

  • The plasma membrane is a highly dynamic organelle and fences off pathogens with considerable efficiency

  • Single particle tracking suggests that Adenovirus type 2 (Ad2) movements on the cell surface lead the virus particles to plasma membrane domains proficient for endocytosis, or recruit endocytic effector proteins while they are in a particular motion mode [11,86]

  • Evidence from single particle tracking experiments has demonstrated that particular motion types on the cell surface support infection

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Summary

Introduction

The plasma membrane is a highly dynamic organelle and fences off pathogens with considerable efficiency. Virus entry: Actin-dependent drifts on filopodia and microvilli, diffusion and confinement. Drifting Motions Occur by Coupling Plasma Membrane Receptors to Retrograde F-Actin Flow

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