{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,24]],"date-time":"2026-10-24T01:42:47Z","timestamp":1792806167382,"version":"4.5.0"},"reference-count":51,"publisher":"Cambridge University Press (CUP)","issue":"8","license":[{"start":{"date-parts":[[2017,11,28]],"date-time":"2017-11-28T00:00:00Z","timestamp":1511827200000},"content-version":"unspecified","delay-in-days":0,"URL":"https:\/\/www.cambridge.org\/core\/terms"}],"content-domain":{"domain":["www.cambridge.org"],"crossmark-restriction":true},"short-container-title":["Parasitology"],"published-print":{"date-parts":[[2018,7]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p><jats:italic>Toxoplasma gondii<\/jats:italic>is an intracellular protozoan parasite that causes toxoplasmosis, a prevalent infection related to abortion, ocular diseases and encephalitis in immuno-compromised individuals. In the untreatable (and life-long) chronic stage of toxoplasmosis, parasitophorous vacuoles (PVs, containing<jats:italic>T. gondii<\/jats:italic>tachyzoites) transform into tissue cysts, containing slow-dividing bradyzoite forms. While acute-stage infection with tachyzoites involves global rearrangement of the host cell cytoplasm, focused on favouring tachyzoite replication, the cytoplasmic architecture of cells infected with cysts had not been described. Here, we characterized (by fluorescence and electron microscopy) the redistribution of host cell structures around<jats:italic>T. gondii<\/jats:italic>cysts, using a<jats:italic>T. gondii<\/jats:italic>strain (EGS) with high rates of spontaneous cystogenesis<jats:italic>in vitro<\/jats:italic>. Microtubules and intermediate filaments (but not actin microfilaments) formed a \u2018cage\u2019 around the cyst, and treatment with taxol (to inhibit microtubule dynamics) favoured cystogenesis. Mitochondria, which appeared adhered to the PV membrane, were less closely associated with the cyst wall. Endoplasmic reticulum (ER) profiles were intimately associated with folds in the cyst wall membrane. However, the Golgi complex was not preferentially localized relative to the cyst, and treatment with tunicamycin or brefeldin A (to disrupt Golgi or ER function, respectively) had no significant effect on cystogenesis. Lysosomes accumulated around cysts, while early and late endosomes were more evenly distributed in the cytoplasm. The endocytosis tracer HRP (but not BSA or transferrin) reached bradyzoites after uptake by infected host cells. These results suggest that<jats:italic>T. gondii<\/jats:italic>cysts reorganize the host cell cytoplasm, which may fulfil specific requirements of the chronic stage of infection.<\/jats:p>","DOI":"10.1017\/s0031182017002050","type":"journal-article","created":{"date-parts":[[2017,11,28]],"date-time":"2017-11-28T09:35:02Z","timestamp":1511861702000},"page":"1027-1038","update-policy":"https:\/\/doi.org\/10.1017\/policypage","source":"Crossref","is-referenced-by-count":15,"title":["<i>Toxoplasma gondii<\/i>reorganizes the host cell architecture during spontaneous cyst formation<i>in vitro<\/i>"],"prefix":"10.1017","volume":"145","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5355-1012","authenticated-orcid":false,"given":"T. C.","family":"Paredes-Santos","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"E. 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