Recently it has been suggested that host cells may utilize autophagy as a defense against intracellular pathogens [16] [17] [18] . Autophagy is a mechanism by which cytoplasmic components, including long-lived proteins and damaged organelles (peroxisomes, ER, and mitochondria) are enveloped within specialized double-membrane-bound vesicles that deliver their cargo to the lysosome for degradation [19] [20] [21] . It has been hypothesized that basal levels of autophagy occur continuously inside of cells [20] . An increase in autophagic activity can be stimulated by amino acid starvation, hormone signaling, cytokines, TLR stimulation, immunity related GTPases and microbial infection [16] [17] [18] 20] . However, the mechanism by which substrates are targeted for autophagic degradation is unknown [20] .