Cell invasion by Theileria sporozoites

Shaw, Michael K.

doi:10.1016/s1471-4922(02)00015-6

Cited by 110 publications

(109 citation statements)

References 22 publications

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“…Plasmodium also harbors micronemes, but in contrast to T. gondii, these appear to be dispensable for egress, at least for blood-stage parasites (56). It remains to be established whether corresponding and/or different secretory organelles operate in related organisms, as has been proposed for rhoptries and microspheres in the escape of the Theileria sporozoite from its vacuole into the lymphocyte cytosol (129).…”

Section: Discussionmentioning

confidence: 99%

Prison Break: Pathogens' Strategies To Egress from Host Cells

Friedrich

Hagedorn

Soldati‐Favre

et al. 2012

Microbiol Mol Biol Rev

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SUMMARYA wide spectrum of pathogenic bacteria and protozoa has adapted to an intracellular life-style, which presents several advantages, including accessibility to host cell metabolites and protection from the host immune system. Intracellular pathogens have developed strategies to enter and exit their host cells while optimizing survival and replication, progression through the life cycle, and transmission. Over the last decades, research has focused primarily on entry, while the exit process has suffered from neglect. However, pathogen exit is of fundamental importance because of its intimate association with dissemination, transmission, and inflammation. Hence, to fully understand virulence mechanisms of intracellular pathogens at cellular and systemic levels, it is essential to consider exit mechanisms to be a key step in infection. Exit from the host cell was initially viewed as a passive process, driven mainly by physical stress as a consequence of the explosive replication of the pathogen. It is now recognized as a complex, strategic process termed “egress,” which is just as well orchestrated and temporally defined as entry into the host and relies on a dynamic interplay between host and pathogen factors. This review compares egress strategies of bacteria, pathogenic yeast, and kinetoplastid and apicomplexan parasites. Emphasis is given to recent advances in the biology of egress in mycobacteria and apicomplexans.

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Section: Discussionmentioning

confidence: 99%

Prison Break: Pathogens' Strategies To Egress from Host Cells

Friedrich

Hagedorn

Soldati‐Favre

et al. 2012

Microbiol Mol Biol Rev

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“…To this regard, the case of Theileria is particularly interesting, as the merozoite and sporozoite stages are nonmotile (with no micronemes), and require neither apical attachment to the host cell nor apical organelle secretion for invasion. Instead, they enter their host cell by a zippering process, which also leads to the formation of a PV (Shaw, 2003). Nevertheless, the genes encoding proteins of the gliding machinery are present in the Theileria genome and so are the components of the MJ (Table 1).…”

Section: One Mj Complex or Several?mentioning

confidence: 99%

The moving junction of apicomplexan parasites: a key structure for invasion

Besteiro¹,

Dubremetz

Lebrun

2011

Cellular Microbiology

265

214

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SummaryMost Apicomplexa are obligate intracellular parasites and many are important pathogens of human and domestic animals. For a successful cell invasion, they rely on their own motility and on a firm anchorage to their host cell, depending on the secretion of proteins and the establishment of a structure called the moving junction (MJ). The MJ moves from the apical to the posterior end of the parasite, leading to the internalization of the parasite into a parasitophorous vacuole. Based on recent data obtained in Plasmodium and Toxoplasma, an emerging model emphasizes a cooperative role of secreted parasitic proteins in building the MJ and driving this crucial invasive process. More precisely, the parasite exports the microneme protein AMA1 to its own surface and the rhoptry neck RON2 protein as a receptor inserted into the host cell together with other RON partners. Ongoing and future research will certainly help refining the model by characterizing the molecular organization within the MJ and its interactions with both host and parasite cytoskeleton for anchoring of the complex.

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“…Why can Theileria thrive without pathways essential to other apicomplexans? One obvious difference is the cytoplasmic niche occupied by this parasite (57). The absence of a PV allows for a more intimate contact with the host cell and might facilitate uptake and/or manipulation of the host pathways to suit the needs of the parasite.…”

Section: What Is the Reason For The Surprising Diversity Of Fatty Acimentioning

confidence: 99%