Figure 23–26 Legionella pneumophila residing in a compartment with characteristics similar to those of the rough endoplasmic reticulum (eR). (A) Electron micrograph showing the unusual coiled structure that the Legionella pneumophila bacterium induces on the surface of a phagocyte during the invasion process. Some other pathogens, including the bacterium Borrelia burgdorferi, which causes Lyme disease, the eukaryotic pathogen Leishmania, and the yeast Candida albicans, can also invade cells using this type of coiling phagocytosis. (B) Following invasion, L. pneumophila uses its type IV secretion system to secrete effector proteins that block phagosome–endosome fusion and phagosome maturation. It also secretes effector proteins that promote the fusion of the phagosome with ER-derived vesicles, thereby creating a Legionella-containing vacuole with characteristics similar to the rough ER. (A, from M.A. Horwitz, Cell 36:27–33, 1984. With permission from Elsevier.) spread to humans by central air-conditioning systems, which harbor infected amoebae and produce microdroplets of water that are easily inhaled. Once in the lung, the bacteria are engulfed by macrophages by an unusual process called coiling phagocytosis (Figure 23–26A). L. pneumophila uses a type IV secretion system to inject effector proteins into the phagocyte that modulate the activity of proteins that regulate vesicular traffic, including SNARE proteins and Rab and Arf family small GTPases (discussed in Chapter 13). The effector proteins thereby prevent the phagosome from fusing with endosomes and promote its fusion with vesicles derived from the endoplasmic reticulum, converting the phagosome into a compartment that resembles the rough endoplasmic reticulum (Figure 23–26B).
Viruses can also alter membrane traffic in the host cell. Enveloped viruses make use of host cell membranes to acquire their own envelope membrane. In the simplest cases, virally encoded glycoproteins are inserted into the endoplasmic reticulum membrane and follow the secretory pathway through the Golgi apparatus to the plasma membrane; the viral capsid proteins and genome assemble into nucleocapsids, which acquire their envelope as they bud off from the plasma membrane (see Figure 23–12). This mechanism is used by many enveloped viruses including HIV-1. Other enveloped viruses such as herpesviruses and vaccinia virus acquire their lipid envelopes in more complex ways (Figure 23–27).
Viruses and Bacteria Use the Host-Cell Cytoskeleton for Intracellular Movement
As mentioned earlier, many pathogens escape into the cytosol rather than remaining in a membrane-enclosed compartment. The cytosol of mammalian cells is extremely viscous, as it is crowded with protein complexes, organelles, and cytoskeletal filaments, all of which inhibit the diffusion of particles the size of a bacterium or a viral nucleocapsid. Thus, to reach a particular region of the host cell a pathogen must be actively moved there. As with transport of intracellular organelles, pathogens generally use the host cell’s cytoskeleton for their active movement.
nucleus Golgi WRAPPING (?) (B)