FIGURE 1.

Cytoskeleton and mechanosensors play crucial roles during viral infections. (A) Actin filaments in host cells participate in virus surfing before entering into the cells. (B) Actin filaments provide forces for viral entry through clathrin-mediated endocytosis. (C) Macropinocytosis is employed by viruses for entry which is an actin-dependent process. (D) Actin monomers undergo rapid polymerization to generate forces for viral entry through caveolae-mediated endocytosis. (E) Microtubule and actin filament motor proteins dynein and myosin may provide forces for virus uncoating, respectively. (F) Actin filaments provide bending force to expel viruses to the extracellular environment. (G) Focal adhesion and FAK can sense extracellular mechanical signals such as shear force (horizonal arrow), tensile forces (slanting arrow), and ECM stiffness (gradient background color). Focal adhesion proteins can also affect viral infection in multiple ways. (H) Cell–cell junctions sense forces from intracellular and extracellular environments, and may be employed by viruses to facilitate their infection. (I) Caveolae sense extracellular stress. The number, morphology, and localization of caveolae are altered in response to stress and further affect viral infection.