Intracellular Pathogens: Host Immunity and Microbial Persistence Strategies

Figure 2

Schematic representation of the mechanisms of persistence of selected intracellular pathogens. Left: an overview of the various mechanisms used by pathogens to overcome innate and adaptive immune responses. The major strategies are discussed in more detail in the text. Right: evasion strategies of various phagocytic mechanisms by selected intracellular pathogens. Viruses such as influenza virus are able to inhibit the activation of antiviral mechanisms, such as the production of interferon upon viral infection, and enter the nucleus. Mycobacterium tuberculosis after phagocytosis acquires the early endosome marker Rab5, which blocks fusion with the lysosome, and the mycobacteria replicate in this early endosome. Legionella pneumophila resides and multiplies in vacuoles that acquire Rab1 and secretes effector molecules via its type IV secretion system, which inhibits phagolysosome formation. Listeria monocytogenes-engulfed phagosome undergoes acidification, which perforates the phagosomal membrane and the bacteria escape into the cytosol, where they move within and then among cells with actin polymerization. Chlamydia spp. are present as nonreplicating infectious “elementary body” and intracytoplasmic replicating noninfectious “reticulate body.” The elementary body induces its own endocytosis upon exposure to host cells and survives and multiplies inside phagolysosome before infecting the new host. Coxiella burnetii and Brucella abortus are present inside a vacuole, which becomes acidic and acquires Rab5 followed by Rab7 that prevents phagolysosome formation. The Francisella tularensis phagosome acquires Rab5 (early endosome) and then Rab7 (late endosome). Late endosome is not acidified, which disrupts the phagosomal membrane discharging the bacteria into the cytosol. These vacuoles fuse with the endoplasmic reticulum, which allow bacterial replication. Leishmania spp. phagosome becomes acidic phagolysosome, which bears Rab7, and the parasite survives and multiplies inside the phagolysosome.