{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,13]],"date-time":"2025-11-13T18:17:07Z","timestamp":1763057827421},"reference-count":37,"publisher":"American Society for Microbiology","issue":"1","license":[{"start":{"date-parts":[[2015,1,1]],"date-time":"2015-01-01T00:00:00Z","timestamp":1420070400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Eukaryot Cell"],"published-print":{"date-parts":[[2015,1]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            Prior to invading nonreplicative erythrocytes,\n            <jats:named-content content-type=\"genus-species\">Plasmodium<\/jats:named-content>\n            parasites undergo their first obligate step in the mammalian host inside hepatocytes, where each sporozoite replicates to generate thousands of merozoites. While normally quiescent, hepatocytes retain proliferative capacity and can readily reenter the cell cycle in response to diverse stimuli. Many intracellular pathogens, including protozoan parasites, manipulate the cell cycle progression of their host cells for their own benefit, but it is not known whether the hepatocyte cell cycle plays a role during\n            <jats:named-content content-type=\"genus-species\">Plasmodium<\/jats:named-content>\n            liver stage infection. Here, we show that\n            <jats:named-content content-type=\"genus-species\">Plasmodium<\/jats:named-content>\n            parasites can be observed in mitotic hepatoma cells throughout liver stage development, where they initially reduce the likelihood of mitosis and ultimately lead to significant acquisition of a binucleate phenotype. However, hepatoma cells pharmacologically arrested in S phase still support robust and complete\n            <jats:named-content content-type=\"genus-species\">Plasmodium<\/jats:named-content>\n            liver stage development, which thus does not require cell cycle progression in the infected cell\n            <jats:italic>in vitro<\/jats:italic>\n            . Furthermore, murine hepatocytes remain quiescent throughout\n            <jats:italic>in vivo<\/jats:italic>\n            infection with either\n            <jats:named-content content-type=\"genus-species\">Plasmodium berghei<\/jats:named-content>\n            or\n            <jats:named-content content-type=\"genus-species\">Plasmodium yoelii<\/jats:named-content>\n            , as do\n            <jats:named-content content-type=\"genus-species\">Plasmodium falciparum<\/jats:named-content>\n            -infected primary human hepatocytes, demonstrating that the rapid and prodigious growth of liver stage parasites is accomplished independent of host hepatocyte cell cycle progression during natural infection.\n          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