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• W2770583059 abstract "Engineered liver systems come in a variety of platform models, from 2-dimensional cocultures of primary human hepatocytes and stem cell–derived progeny, to 3-dimensional organoids and humanized mice. Because of the species-specificity of many human hepatropic pathogens, these engineered systems have been essential tools for biologic discovery and therapeutic agent development in the context of liver-dependent infectious diseases. Although improvement of existing models is always beneficial, and the addition of a robust immune component is a particular need, at present, considerable progress has been made using this combination of research platforms. We highlight advances in the study of hepatitis B and C viruses and malaria-causing Plasmodium falciparum and Plasmodium vivax parasites, and underscore the importance of pairing the most appropriate model system and readout modality with the particular experimental question at hand, without always requiring a platform that recapitulates human physiology in its entirety. Engineered liver systems come in a variety of platform models, from 2-dimensional cocultures of primary human hepatocytes and stem cell–derived progeny, to 3-dimensional organoids and humanized mice. Because of the species-specificity of many human hepatropic pathogens, these engineered systems have been essential tools for biologic discovery and therapeutic agent development in the context of liver-dependent infectious diseases. Although improvement of existing models is always beneficial, and the addition of a robust immune component is a particular need, at present, considerable progress has been made using this combination of research platforms. We highlight advances in the study of hepatitis B and C viruses and malaria-causing Plasmodium falciparum and Plasmodium vivax parasites, and underscore the importance of pairing the most appropriate model system and readout modality with the particular experimental question at hand, without always requiring a platform that recapitulates human physiology in its entirety. SummaryThis article discusses existing 2-dimensional and 3-dimensional liver models and their applications toward studying hepatotropic pathogens. The importance of selecting the most appropriate models and readout modalities to answer specific scientific questions is emphasized. This article discusses existing 2-dimensional and 3-dimensional liver models and their applications toward studying hepatotropic pathogens. The importance of selecting the most appropriate models and readout modalities to answer specific scientific questions is emphasized. The liver is the largest internal organ in the body, and performs vital and diverse functions in metabolism of carbohydrates, proteins, and lipids; bioproduct synthesis; immunologic processes; and detoxification. Although many viruses, parasites, and bacteria specifically target the cells of the liver, the liver is also exposed to blood-borne pathogens that circulate systemically, or that are derived from the gut,1Jenne C.N. Kubes P. Immune surveillance by the liver.Nat Immunol. 2013; 14: 996-1006Crossref PubMed Scopus (187) Google Scholar because of its location at the convergence of the hepatic artery and portal vein. Most liver pathogens specifically target the most abundant cell type in the liver, the hepatocyte, for completion of their life cycles or developmental stages. These include hepatitis viruses and Plasmodium protozoan parasites (Figure 1), which together account for an enormous burden on human health. Hepatitis B virus (HBV) and hepatitis C virus (HCV) infect the livers of more than 350 million people worldwide, and are the main causes for chronic liver diseases, such as liver cirrhosis and hepatocellular carcinoma.2Protzer U. Maini M.K. Knolle P.A. Living in the liver: hepatic infections.Nat Rev Immunol. 2012; 12: 201-213Crossref PubMed Scopus (183) Google Scholar Plasmodium parasites, which cause malaria, result in more than 200 million infections annually3World Health OrganizationWorld malaria report 2016. WHO, Geneva2017Google Scholar and require asymptomatic development in the liver before initiating fevers associated with blood stage infection. 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