Component of the Dot/Icm type IVB secretion system (T4BSS), which is used to inject bacterial effector proteins into eukaryotic host cells (PubMed:15661013, PubMed:18069892, PubMed:17040490, PubMed:22694730, PubMed:32513920). Part of a subcomplex which recruits effector proteins and delivers them to the core transmembrane subcomplex (PubMed:23028312, PubMed:32513920). The IcmS/IcmW protein complex plays an important role in protein translocation by interacting with multiple Dot/Icm effector proteins to facilitate their translocation into host cells (PubMed:15661013, PubMed:18069892). Interaction promotes conformational changes in the effector protein, which may facilitate display of a C-terminal translocation signal (PubMed:18069892). May maintain the substrates in a translocation competent form (PubMed:23028312). Required for intracellular growth in host cells, replicative phagosome formation and phagosome trafficking (PubMed:11115108). IcmS is required for IcmW stability (PubMed:15661013, PubMed:29203674). Interaction with DotL is critical for the export of IcmSW-dependent substrates. The T4BSS is a complex nanomachine composed of several subcomplexes. This subunit is part of the Type IV Coupling Complex (T4CC), a subcomplex composed of the DotLMNYZ core and the IcmSW-LvgA adapter subunits, linked by the C-terminal tail of DotL (PubMed:17040490, PubMed:22694730, PubMed:28714967, PubMed:32457311, PubMed:32513920). Interacts with IcmW (PubMed:11115108, PubMed:15661013, PubMed:29203674). IcmS and IcmW form a stable complex (PubMed:15661013). Interacts directly with the type 4 coupling protein DotL (PubMed:23028312, PubMed:29203674, PubMed:32513920). Interacts with LvgA (PubMed:29203674, PubMed:16803597). Interacts with effector proteins (PubMed:18069892, PubMed:29203674). Associates with the inner membrane at the poles in a DotL/DotM/DotN-dependent manner. Deletion of the gene leads to a strong decrease in intracellular growth in human monocytes (PubMed:11115108). Mutant is unable to evade phagosome lysosome fusion, but retains the pore-forming activity (PubMed:11115108). Mutation severely impairs the translocation into host cells of multiple effector proteins, including SidA, SidB, SidC, SidD, SidE, SidG, SidH, WipA and WipB (PubMed:15661013, PubMed:18069892). Loss of this gene has a profound effect on the levels of IcmW (PubMed:17040490).