*2.2.6 Crosstalk between SPI-1 and SPI-2 gene products to promote Salmonella survival and virulence*

The SPI-2 genes are activated after *Salmonella* gains access into the SCV [76]. T3SS-2 secretes multiple effector proteins into different subcellular fractions where they interfere with various host cellular functions to establish a replication-permissive environment [90]. The identified effectors are encoded within SPI-2 (e.g., SpiC, SseF and SseG) and outside SPI-2 (e.g., SifA, SseI, SseJ and SspH 2) [23]. These SPI-2-encoded effectors together with some of SPI-1-encoded effectors (e.g., SipA, SipD, SopA, SopE, SopB) that persist in the host cytosol after invasion, are distributed in different cellular compartments including the vascular membrane of SCV and Sif, host cytosol, cytoskeleton, Golgi apparatus, and nucleus. These molecules influence distinct intracellular events and collectively contribute to establish a *Salmonella* replicative niche in macrophages [91]. These intracellular events include: inhibition of endocytic trafficking, evasion of NADPH oxidase-dependent killing [92, 93], induction of a delayed apoptosis-like host cell death [94], assembly of a meshwork of F-actin around the SCV [59], accumulation of cholesterol in the SCV [95], and interference with the localization of inducible nitric oxide synthase to the SCV [96]. Efficient replication has been found to be associated with two phenotypes involving host microtubule cytoskeleton and its motor proteins, Golgi apparatus-associated juxtanuclear positioning of SCV [97–99] and Sifs formation which appear as tubular membrane extensions of SCVs enriched in lysosomal glycan proteins [100].
