Table 3.

Pathogens and actin interaction

Pathogen	Mechanism of action adaptation in host cell	References
Salmonella spp.	Translocate effectors (SopE and SopE2) into host cells which increase F actin polymerization.	[133, 134, 137]
Listeria monocytogenes	ActA protein recruits an Arp2/3 on the surface of listeria which promotes actin polymerization that helps in the movement of bacteria in the cells.	[139, 140]
E. coli	Actin-rich filament that facilitates their attachment.	[141, 142]
Chlamydia trachomatis	Secrete actin-recruiting phosphoprotein (Tarp) which cause actin polymerization depolymerization in the host cell.	[143, 144]
Coxiella burnetii	Infects phagocytic human macrophages via binding to complement receptor 3 (CR3) receptors, triggering the reorganization of filamentous actin at the attachment site.	[145]
Rickettsia conorii	Attachment to host cell requires actin rearrangement via recruitment and activation of Arp2/3.	[146]
Tick-borne pathogen Anaplasma phagocytophilu	Actin polymerization at invasion.	[147]
Ehrlichia chaffeensis	Manipulation of cytoskeleton through SUMOylation-dependent protein-protein interactions between bacterial effectors and host cytoskeletal components.	[148]
Vaccinia viruses	Receptor tyrosine kinase signaling which in turn ignite actin polymerization through N-WASP-Arp2/3 cascade.	[149]