text: R. rickettsii is also able to suppress immune responses while dwelling in infected cells by creating inhibitory proteins such as Rickettsial ankyrin repeat protein 2 (RARP2). RARP2 mediates the fragmentation of TGN, or the trans-Golgi network, causing attenuation of vesicular transport and glycosylation defects in infected host cells. There are two important proteins within the host cell that are affected by these glycosylation defects: TGN46 and major histocompatibility complex class 1 (MHC-I). MHC-I is an important protein for defending against pathogens as it functions as an antigen presenting complex signaling its infection status to lyphocytes. However, since RARP2 causes attenuation of vesicular transport, MHC-I is unable to be transported to the plasma membrane and the infected cell will not be able to alert host immune cells. Thus, the bacterial cells are able to avoid certain immune responses and allow for proliferation within a host cell.
  Genome and phenotypes
  R. rickettsii is an obligate intracellular alpha proteobacterium that belongs to the Rickettsiacea family. It has a genome that consists of about 1.27 Mbp with ~1,350 predicted genes, which is smaller compared to most other bacteria. This small genome size allows the bacteria to maintain an intracellular lifestyle with increased pathogenicity from gene reduction. It is maintained in its tick host by transovarial transmission. The multiplication of R. rickettsii is by binary fission inside the cytosol.