Intracellular bacteria and viruses often comprise a group of highly infectious pathogens that can cause several diseases. Bacterial pathogens include those belonging to the genus Rickettsia responsible for conditions such as rocky mountain spotted fever and the Mediterranean spotted fever; Chlamydia, a genus responsible for a sexually transmitted disease; Coxiella burnetii, an agent responsible for Q fever. Viral pathogens include vaccinia—a poxvirus, and herpes simplex virus—a virus that causes contagious sores.

These bacteria and viruses rely on the host cell's cytoskeleton for their intracellular movement from the cell surface to the nuclear region and vice versa, and across different cells through the cortical protrusions. These organisms have evolved numerous mechanisms to navigate the host cytoskeleton and facilitate infection. They could depend on cellular motors moving on a combination of microtubule and actin filament tracks or actin filaments' polymerization. The following example will discuss the mechanism of bacterial intracellular transport in detail.

Intracellular Transport Mechanism of Rickettsia

Bacteria such as R. rickettsii and R. conorii stimulate actin polymerization to form an actin tail for their motility within the cell. After these bacteria enter the cell, the actin polymerizing protein RickA localizes to the bacterial pole. RickA contains a WH2 domain with a binding site for actin monomers and WASP proteins that regulate the Arp2/3 complex. Arp2/3 complex, a nucleation factor, promotes actin polymerization. Once the actin filament polymerization is initiated, it allows the early slow movement of bacteria through the cytoplasm. At a later stage of infection, the rickettsial autotransporter Sca2 resembles host formin homology proteins, responsible for elongation of pre-existing actin filament by removing capping proteins. This copying of elongation machinery forms an actin tail that results in the bacteria's rapid and directional motility, transporting it across the cell.