Intracellular Movement of Viruses and Bacteria

Bacteria express surface proteins that activate the Arp2/3 complex, initiating assembly of host actin filaments into tails. These growing tails generate thrust, propelling the bacterium forward through the cytoplasm. This actin polymerization-based movement allows bacteria to navigate the viscous cytosol and overcome resistance from organelles and protein complexes.

Viruses entering neurons lose their lipid envelope, and the protein-coated viral particle is carried by dynein motor proteins into the nucleus. After replication, kinesin motor proteins transport virus particles to the axonal tip for release or movement into neighboring cells. This microtubule-motor protein-based movement enables efficient viral trafficking through the cell.

Rickettsia bacteria initially use RickA protein to stimulate actin polymerization for slow movement. Later, the rickettsial autotransporter Sca2 resembles host formin proteins, elongating pre-existing actin filaments by removing capping proteins. This generates an actin tail enabling rapid, directional motility that transports bacteria across the cell.

The cytosol is viscous and filled with organelles and protein complexes that hinder free movement. Cytoskeletal proteins like actins and tubulins provide structural tracks and polymerization mechanisms that pathogens exploit for navigation. These proteins enable bacteria and viruses to move efficiently from the cell surface to the nucleus and across neighboring cells.

The Arp2/3 complex acts as a nucleation factor that promotes actin polymerization when activated by bacterial surface proteins. It initiates assembly of branched actin filaments that form tails behind the bacterium. The generation of straight or branched actin filaments creates the mechanical force necessary for bacterial propulsion through the host cell.

Bacteria and viruses move through cortical protrusions using cytoskeletal tracks composed of microtubules and actin filaments. They exploit the role of actin and myosin in non-muscle cells to facilitate intercellular transport. These pathogens have evolved mechanisms to hijack host cytoskeletal machinery, enabling them to spread infection across multiple cells.

Rickettsia bacteria cause rocky mountain spotted fever and Mediterranean spotted fever. Chlamydia causes sexually transmitted disease, while Coxiella burnetii causes Q fever. Viral pathogens include vaccinia virus and herpes simplex virus, which causes contagious sores. These highly infectious pathogens rely on cytoskeletal hijacking for their pathogenesis.