A Human Lung Xenograft Mouse Model of Nipah Virus Infection
Nipah virus (NiV) is a member of the genus Henipavirus (family Paramyxoviridae) that causes severe and often lethal respiratory illness and encephalitis in humans with high mortality rates (up to 92%). NiV can cause Acute Lung Injury (ALI) in humans, and human-to-human transmission has been observed...
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| Published in | PLoS pathogens Vol. 10; no. 4; p. e1004063 |
|---|---|
| Main Authors | , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Public Library of Science
01.04.2014
Public Library of Science (PLoS) |
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| Abstract | Nipah virus (NiV) is a member of the genus Henipavirus (family Paramyxoviridae) that causes severe and often lethal respiratory illness and encephalitis in humans with high mortality rates (up to 92%). NiV can cause Acute Lung Injury (ALI) in humans, and human-to-human transmission has been observed in recent outbreaks of NiV. While the exact route of transmission to humans is not known, we have previously shown that NiV can efficiently infect human respiratory epithelial cells. The molecular mechanisms of NiV-associated ALI in the human respiratory tract are unknown. Thus, there is an urgent need for models of henipavirus infection of the human respiratory tract to study the pathogenesis and understand the host responses. Here, we describe a novel human lung xenograft model in mice to study the pathogenesis of NiV. Following transplantation, human fetal lung xenografts rapidly graft and develop mature structures of adult lungs including cartilage, vascular vessels, ciliated pseudostratified columnar epithelium, and primitive "air" spaces filled with mucus and lined by cuboidal to flat epithelium. Following infection, NiV grows to high titers (10(7) TCID50/gram lung tissue) as early as 3 days post infection (pi). NiV targets both the endothelium as well as respiratory epithelium in the human lung tissues, and results in syncytia formation. NiV infection in the human lung results in the production of several cytokines and chemokines including IL-6, IP-10, eotaxin, G-CSF and GM-CSF on days 5 and 7 pi. In conclusion, this study demonstrates that NiV can replicate to high titers in a novel in vivo model of the human respiratory tract, resulting in a robust inflammatory response, which is known to be associated with ALI. This model will facilitate progress in the fundamental understanding of henipavirus pathogenesis and virus-host interactions; it will also provide biologically relevant models for other respiratory viruses. |
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| AbstractList | Nipah virus (NiV) is a member of the genus Henipavirus (family Paramyxoviridae) that causes severe and often lethal respiratory illness and encephalitis in humans with high mortality rates (up to 92%). NiV can cause Acute Lung Injury (ALI) in humans, and human-to-human transmission has been observed in recent outbreaks of NiV. While the exact route of transmission to humans is not known, we have previously shown that NiV can efficiently infect human respiratory epithelial cells. The molecular mechanisms of NiV-associated ALI in the human respiratory tract are unknown. Thus, there is an urgent need for models of henipavirus infection of the human respiratory tract to study the pathogenesis and understand the host responses. Here, we describe a novel human lung xenograft model in mice to study the pathogenesis of NiV. Following transplantation, human fetal lung xenografts rapidly graft and develop mature structures of adult lungs including cartilage, vascular vessels, ciliated pseudostratified columnar epithelium, and primitive "air" spaces filled with mucus and lined by cuboidal to flat epithelium. Following infection, NiV grows to high titers (10(7) TCID50/gram lung tissue) as early as 3 days post infection (pi). NiV targets both the endothelium as well as respiratory epithelium in the human lung tissues, and results in syncytia formation. NiV infection in the human lung results in the production of several cytokines and chemokines including IL-6, IP-10, eotaxin, G-CSF and GM-CSF on days 5 and 7 pi. In conclusion, this study demonstrates that NiV can replicate to high titers in a novel in vivo model of the human respiratory tract, resulting in a robust inflammatory response, which is known to be associated with ALI. This model will facilitate progress in the fundamental understanding of henipavirus pathogenesis and virus-host interactions; it will also provide biologically relevant models for other respiratory viruses.Nipah virus (NiV) is a member of the genus Henipavirus (family Paramyxoviridae) that causes severe and often lethal respiratory illness and encephalitis in humans with high mortality rates (up to 92%). NiV can cause Acute Lung Injury (ALI) in humans, and human-to-human transmission has been observed in recent outbreaks of NiV. While the exact route of transmission to humans is not known, we have previously shown that NiV can efficiently infect human respiratory epithelial cells. The molecular mechanisms of NiV-associated ALI in the human respiratory tract are unknown. Thus, there is an urgent need for models of henipavirus infection of the human respiratory tract to study the pathogenesis and understand the host responses. Here, we describe a novel human lung xenograft model in mice to study the pathogenesis of NiV. Following transplantation, human fetal lung xenografts rapidly graft and develop mature structures of adult lungs including cartilage, vascular vessels, ciliated pseudostratified columnar epithelium, and primitive "air" spaces filled with mucus and lined by cuboidal to flat epithelium. Following infection, NiV grows to high titers (10(7) TCID50/gram lung tissue) as early as 3 days post infection (pi). NiV targets both the endothelium as well as respiratory epithelium in the human lung tissues, and results in syncytia formation. NiV infection in the human lung results in the production of several cytokines and chemokines including IL-6, IP-10, eotaxin, G-CSF and GM-CSF on days 5 and 7 pi. In conclusion, this study demonstrates that NiV can replicate to high titers in a novel in vivo model of the human respiratory tract, resulting in a robust inflammatory response, which is known to be associated with ALI. This model will facilitate progress in the fundamental understanding of henipavirus pathogenesis and virus-host interactions; it will also provide biologically relevant models for other respiratory viruses. Nipah virus (NiV) is a member of the genus Henipavirus (family Paramyxoviridae) that causes severe and often lethal respiratory illness and encephalitis in humans with high mortality rates (up to 92%). NiV can cause Acute Lung Injury (ALI) in humans, and human-to-human transmission has been observed in recent outbreaks of NiV. While the exact route of transmission to humans is not known, we have previously shown that NiV can efficiently infect human respiratory epithelial cells. The molecular mechanisms of NiV-associated ALI in the human respiratory tract are unknown. Thus, there is an urgent need for models of henipavirus infection of the human respiratory tract to study the pathogenesis and understand the host responses. Here, we describe a novel human lung xenograft model in mice to study the pathogenesis of NiV. Following transplantation, human fetal lung xenografts rapidly graft and develop mature structures of adult lungs including cartilage, vascular vessels, ciliated pseudostratified columnar epithelium, and primitive "air" spaces filled with mucus and lined by cuboidal to flat epithelium. Following infection, NiV grows to high titers (107 TCID50/gram lung tissue) as early as 3 days post infection (pi). NiV targets both the endothelium as well as respiratory epithelium in the human lung tissues, and results in syncytia formation. NiV infection in the human lung results in the production of several cytokines and chemokines including IL-6, IP-10, eotaxin, G-CSF and GM-CSF on days 5 and 7 pi. In conclusion, this study demonstrates that NiV can replicate to high titers in a novel in vivo model of the human respiratory tract, resulting in a robust inflammatory response, which is known to be associated with ALI. This model will facilitate progress in the fundamental understanding of henipavirus pathogenesis and virus-host interactions; it will also provide biologically relevant models for other respiratory viruses. Nipah virus (NiV) is a member of the genus Henipavirus (family Paramyxoviridae) that causes severe and often lethal respiratory illness and encephalitis in humans with high mortality rates (up to 92%). NiV can cause Acute Lung Injury (ALI) in humans, and human-to-human transmission has been observed in recent outbreaks of NiV. While the exact route of transmission to humans is not known, we have previously shown that NiV can efficiently infect human respiratory epithelial cells. The molecular mechanisms of NiV-associated ALI in the human respiratory tract are unknown. Thus, there is an urgent need for models of henipavirus infection of the human respiratory tract to study the pathogenesis and understand the host responses. Here, we describe a novel human lung xenograft model in mice to study the pathogenesis of NiV. Following transplantation, human fetal lung xenografts rapidly graft and develop mature structures of adult lungs including cartilage, vascular vessels, ciliated pseudostratified columnar epithelium, and primitive "air" spaces filled with mucus and lined by cuboidal to flat epithelium. Following infection, NiV grows to high titers (10(7) TCID50/gram lung tissue) as early as 3 days post infection (pi). NiV targets both the endothelium as well as respiratory epithelium in the human lung tissues, and results in syncytia formation. NiV infection in the human lung results in the production of several cytokines and chemokines including IL-6, IP-10, eotaxin, G-CSF and GM-CSF on days 5 and 7 pi. In conclusion, this study demonstrates that NiV can replicate to high titers in a novel in vivo model of the human respiratory tract, resulting in a robust inflammatory response, which is known to be associated with ALI. This model will facilitate progress in the fundamental understanding of henipavirus pathogenesis and virus-host interactions; it will also provide biologically relevant models for other respiratory viruses. Nipah virus (NiV) is a member of the genus Henipavirus (family Paramyxoviridae) that causes severe and often lethal respiratory illness and encephalitis in humans with high mortality rates (up to 92%). NiV can cause Acute Lung Injury (ALI) in humans, and human-to-human transmission has been observed in recent outbreaks of NiV. While the exact route of transmission to humans is not known, we have previously shown that NiV can efficiently infect human respiratory epithelial cells. The molecular mechanisms of NiV-associated ALI in the human respiratory tract are unknown. Thus, there is an urgent need for models of henipavirus infection of the human respiratory tract to study the pathogenesis and understand the host responses. Here, we describe a novel human lung xenograft model in mice to study the pathogenesis of NiV. Following transplantation, human fetal lung xenografts rapidly graft and develop mature structures of adult lungs including cartilage, vascular vessels, ciliated pseudostratified columnar epithelium, and primitive "air" spaces filled with mucus and lined by cuboidal to flat epithelium. Following infection, NiV grows to high titers ([10.sup.7] [TCID.sub.50]/gram lung tissue) as early as 3 days post infection (pi). NiV targets both the endothelium as well as respiratory epithelium in the human lung tissues, and results in syncytia formation. NiV infection in the human lung results in the production of several cytokines and chemokines including IL-6, IP-10, eotaxin, G-CSF and GM-CSF on days 5 and 7 pi. In conclusion, this study demonstrates that NiV can replicate to high titers in a novel in vivo model of the human respiratory tract, resulting in a robust inflammatory response, which is known to be associated with ALI. This model will facilitate progress in the fundamental understanding of henipavirus pathogenesis and virus-host interactions; it will also provide biologically relevant models for other respiratory viruses. Nipah virus (NiV) is a member of the genus Henipavirus (family Paramyxoviridae ) that causes severe and often lethal respiratory illness and encephalitis in humans with high mortality rates (up to 92%). NiV can cause Acute Lung Injury (ALI) in humans, and human-to-human transmission has been observed in recent outbreaks of NiV. While the exact route of transmission to humans is not known, we have previously shown that NiV can efficiently infect human respiratory epithelial cells. The molecular mechanisms of NiV-associated ALI in the human respiratory tract are unknown. Thus, there is an urgent need for models of henipavirus infection of the human respiratory tract to study the pathogenesis and understand the host responses. Here, we describe a novel human lung xenograft model in mice to study the pathogenesis of NiV. Following transplantation, human fetal lung xenografts rapidly graft and develop mature structures of adult lungs including cartilage, vascular vessels, ciliated pseudostratified columnar epithelium, and primitive “air” spaces filled with mucus and lined by cuboidal to flat epithelium. Following infection, NiV grows to high titers (10 7 TCID 50 /gram lung tissue) as early as 3 days post infection (pi). NiV targets both the endothelium as well as respiratory epithelium in the human lung tissues, and results in syncytia formation. NiV infection in the human lung results in the production of several cytokines and chemokines including IL-6, IP-10, eotaxin, G-CSF and GM-CSF on days 5 and 7 pi. In conclusion, this study demonstrates that NiV can replicate to high titers in a novel in vivo model of the human respiratory tract, resulting in a robust inflammatory response, which is known to be associated with ALI. This model will facilitate progress in the fundamental understanding of henipavirus pathogenesis and virus-host interactions; it will also provide biologically relevant models for other respiratory viruses. Nipah virus (NiV) is a highly pathogenic zoonotic virus that causes fatal disease in humans and a variety of other mammalian hosts including pigs. Given the lack of effective therapeutics and vaccines, this virus is considered a public health and agricultural concern, and listed as category C priority pathogen for biodefense research by the National Institute of Allergy and Infectious Diseases. Both animal-to-human and human-to-human transmission has been observed. Studies on the molecular mechanisms of NiV-mediated pathogenesis have been hampered by the lack of biologically relevant in vivo models for studying the initial host responses to NiV infection in the human lung. We show here a new small animal model in which we transplant human lung tissue for studying the pathogenesis of NiV. We showed that NiV can replicate to high levels in the human lung. NiV causes extensive damage to the lung tissue and induces important regulators of the inflammatory response. This study is the first to use a human lung transplant for studying infectious diseases, a powerful model for studying the pathogenesis of NiV infection, and will open up new possibilities for studying virus-host interactions. |
| Audience | Academic |
| Author | Valbuena, Gustavo Halliday, Hailey Rockx, Barry Borisevich, Viktoriya Goez, Yenny |
| AuthorAffiliation | 1 Department of Pathology, University of Texas Medical Branch, Galveston, Texas, United States of America Johns Hopkins University, United States of America 2 Institute of Human Infections and Immunity, University of Texas Medical Branch, Galveston, Texas, United States of America 3 Department Microbiology & Immunology, University of Texas Medical Branch, Galveston, Texas, United States of America |
| AuthorAffiliation_xml | – name: Johns Hopkins University, United States of America – name: 2 Institute of Human Infections and Immunity, University of Texas Medical Branch, Galveston, Texas, United States of America – name: 1 Department of Pathology, University of Texas Medical Branch, Galveston, Texas, United States of America – name: 3 Department Microbiology & Immunology, University of Texas Medical Branch, Galveston, Texas, United States of America |
| Author_xml | – sequence: 1 givenname: Gustavo surname: Valbuena fullname: Valbuena, Gustavo – sequence: 2 givenname: Hailey surname: Halliday fullname: Halliday, Hailey – sequence: 3 givenname: Viktoriya surname: Borisevich fullname: Borisevich, Viktoriya – sequence: 4 givenname: Yenny surname: Goez fullname: Goez, Yenny – sequence: 5 givenname: Barry surname: Rockx fullname: Rockx, Barry |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/24699832$$D View this record in MEDLINE/PubMed |
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| Cites_doi | 10.3201/eid1012.040701 10.1371/journal.pntd.0002024 10.1016/S0002-9440(10)63569-9 10.1371/journal.pone.0063331 10.1128/JVI.00473-11 10.1371/journal.pone.0040308 10.1016/j.ajpath.2013.06.023 10.1371/journal.ppat.1000642 10.1038/nbt1210-1248 10.3201/eid1307.061128 10.1136/thx.2005.040204 10.3201/eid1812.120875 10.1016/S0002-9440(10)64493-8 10.1093/infdis/jis653 10.1086/529147 10.1002/smll.200801572 10.1126/scitranslmed.3004241 10.1046/j.1432-0436.1995.5850361.x 10.1016/j.virol.2010.05.005 10.1016/S0140-6736(99)04299-3 10.1073/pnas.93.7.3126 10.1016/j.antiviral.2012.05.008 10.1016/j.virusres.2007.02.014 10.1016/S0016-5085(03)00902-8 10.3855/jidc.3648 10.1378/chest.107.4.1062 10.1128/JVI.00549-11 10.1371/journal.pone.0010690 10.4049/jimmunol.154.1.180 10.1160/TH09-05-0310 10.1186/1743-422X-5-142 10.1111/j.1600-6143.2012.04018.x 10.1073/pnas.0813234106 10.1128/JVI.02576-12 10.1378/chest.111.5.1306 10.1128/JVI.00127-09 10.1016/S0140-6736(99)04379-2 |
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| Copyright | COPYRIGHT 2014 Public Library of Science 2014 Valbuena et al 2014 Valbuena et al 2014 Valbuena et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited: Valbuena G, Halliday H, Borisevich V, Goez Y, Rockx B (2014) A Human Lung Xenograft Mouse Model of Nipah Virus Infection. PLoS Pathog 10(4): e1004063. doi:10.1371/journal.ppat.1004063 |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 The authors have declared that no competing interests exist. Conceived and designed the experiments: GV BR. Performed the experiments: GV HH VB YG BR. Analyzed the data: GV BR. Wrote the paper: GV BR. |
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| References | S Erbar (ref10) 2008; 5 AS Headley (ref37) 1997; 111 S Abele-Ohl (ref22) 2012; 12 BA Clayton (ref25) 2012; 18 J Dups (ref29) 2012; 7 R Gao (ref31) 2013; 183 GU Meduri (ref36) 1995; 107 MK Lo (ref9) 2010; 404 VP Hsu (ref4) 2004; 10 M Uhlen (ref23) 2010; 28 MJ Hossain (ref6) 2008; 46 B Rockx (ref13) 2011; 85 A Maisner (ref11) 2009; 102 KN Bossart (ref14) 2012; 4 KT Wong (ref17) 2003; 163 O Escaffre (ref12) 2013; 87 TR Kollmann (ref21) 1996; 93 TW Geisbert (ref16) 2010; 5 ES Gurley (ref5) 2007; 13 KT Wong (ref8) 2002; 161 C Mathieu (ref27) 2011; 85 KN Bossart (ref15) 2009; 5 TC Savidge (ref20) 2003; 125 JE Podesta (ref18) 2009; 5 KB Chua (ref2) 1999; 354 B Rockx (ref1) 2012; 95 LD Shultz (ref24) 1995; 154 BL DeBuysscher (ref26) 2013; 7 B Rockx (ref30) 2009; 83 KP Dhondt (ref28) 2013; 207 CR Baskin (ref32) 2009; 106 O Escaffre (ref7) 2013; 7 MJ Cameron (ref33) 2008; 133 AR Medford (ref34) 2006; 61 VE Calderon (ref35) 2013; 8 NI Paton (ref3) 1999; 354 TC Savidge (ref19) 1995; 58 |
| References_xml | – volume: 10 start-page: 2082 year: 2004 ident: ref4 article-title: Nipah virus encephalitis reemergence, Bangladesh publication-title: Emerg Infect Dis doi: 10.3201/eid1012.040701 – volume: 7 start-page: e2024 year: 2013 ident: ref26 article-title: Comparison of the pathogenicity of Nipah virus isolates from Bangladesh and Malaysia in the Syrian hamster publication-title: PLoS Negl Trop Dis doi: 10.1371/journal.pntd.0002024 – volume: 163 start-page: 2127 year: 2003 ident: ref17 article-title: A golden hamster model for human acute Nipah virus infection publication-title: Am J Pathol doi: 10.1016/S0002-9440(10)63569-9 – volume: 8 start-page: e63331 year: 2013 ident: ref35 article-title: A humanized mouse model of tuberculosis publication-title: PLoS One doi: 10.1371/journal.pone.0063331 – volume: 85 start-page: 7658 year: 2011 ident: ref13 article-title: Clinical outcome of henipavirus infection in hamsters is determined by the route and dose of infection publication-title: J Virol doi: 10.1128/JVI.00473-11 – volume: 7 start-page: e40308 year: 2012 ident: ref29 article-title: A new model for Hendra virus encephalitis in the mouse publication-title: PLoS One doi: 10.1371/journal.pone.0040308 – volume: 183 start-page: 1258 year: 2013 ident: ref31 article-title: Cytokine and chemokine profiles in lung tissues from fatal cases of 2009 pandemic influenza A (H1N1): role of the host immune response in pathogenesis publication-title: Am J Pathol doi: 10.1016/j.ajpath.2013.06.023 – volume: 5 start-page: e1000642 year: 2009 ident: ref15 article-title: A neutralizing human monoclonal antibody protects against lethal disease in a new ferret model of acute nipah virus infection publication-title: PLoS Pathog doi: 10.1371/journal.ppat.1000642 – volume: 28 start-page: 1248 year: 2010 ident: ref23 article-title: Towards a knowledge-based Human Protein Atlas publication-title: Nat Biotechnol doi: 10.1038/nbt1210-1248 – volume: 13 start-page: 1031 year: 2007 ident: ref5 article-title: Person-to-person transmission of Nipah virus in a Bangladeshi community publication-title: Emerg Infect Dis doi: 10.3201/eid1307.061128 – volume: 61 start-page: 621 year: 2006 ident: ref34 article-title: Vascular endothelial growth factor (VEGF) in acute lung injury (ALI) and acute respiratory distress syndrome (ARDS): paradox or paradigm? publication-title: Thorax doi: 10.1136/thx.2005.040204 – volume: 18 start-page: 1983 year: 2012 ident: ref25 article-title: Transmission Routes for Nipah Virus from Malaysia and Bangladesh publication-title: Emerg Infect Dis doi: 10.3201/eid1812.120875 – volume: 161 start-page: 2153 year: 2002 ident: ref8 article-title: Nipah Virus Infection: Pathology and Pathogenesis of an Emerging Paramyxoviral Zoonosis publication-title: The American journal of pathology doi: 10.1016/S0002-9440(10)64493-8 – volume: 207 start-page: 142 year: 2013 ident: ref28 article-title: Type I interferon signaling protects mice from lethal henipavirus infection publication-title: J Infect Dis doi: 10.1093/infdis/jis653 – volume: 46 start-page: 977 year: 2008 ident: ref6 article-title: Clinical presentation of nipah virus infection in Bangladesh publication-title: Clin Infect Dis doi: 10.1086/529147 – volume: 5 start-page: 1176 year: 2009 ident: ref18 article-title: Antitumor activity and prolonged survival by carbon-nanotube-mediated therapeutic siRNA silencing in a human lung xenograft model publication-title: Small doi: 10.1002/smll.200801572 – volume: 4 start-page: 146ra107 year: 2012 ident: ref14 article-title: A Hendra virus G glycoprotein subunit vaccine protects African green monkeys from Nipah virus challenge publication-title: Sci Transl Med doi: 10.1126/scitranslmed.3004241 – volume: 58 start-page: 361 year: 1995 ident: ref19 article-title: Human intestinal development in a severe-combined immunodeficient xenograft model publication-title: Differentiation doi: 10.1046/j.1432-0436.1995.5850361.x – volume: 404 start-page: 78 year: 2010 ident: ref9 article-title: Characterization of the antiviral and inflammatory responses against Nipah virus in endothelial cells and neurons publication-title: Virology doi: 10.1016/j.virol.2010.05.005 – volume: 354 start-page: 1257 year: 1999 ident: ref2 article-title: Fatal encephalitis due to Nipah virus among pig-farmers in Malaysia publication-title: Lancet doi: 10.1016/S0140-6736(99)04299-3 – volume: 93 start-page: 3126 year: 1996 ident: ref21 article-title: Inhibition of acute in vivo human immunodeficiency virus infection by human interleukin 10 treatment of SCID mice implanted with human fetal thymus and liver publication-title: Proc Natl Acad Sci U S A doi: 10.1073/pnas.93.7.3126 – volume: 95 start-page: 135 year: 2012 ident: ref1 article-title: Recent progress in henipavirus research: molecular biology, genetic diversity, animal models publication-title: Antiviral Res doi: 10.1016/j.antiviral.2012.05.008 – volume: 133 start-page: 13 year: 2008 ident: ref33 article-title: Human immunopathogenesis of severe acute respiratory syndrome (SARS) publication-title: Virus Res doi: 10.1016/j.virusres.2007.02.014 – volume: 125 start-page: 413 year: 2003 ident: ref20 article-title: Clostridium difficile toxin B is an inflammatory enterotoxin in human intestine publication-title: Gastroenterology doi: 10.1016/S0016-5085(03)00902-8 – volume: 7 start-page: 308 year: 2013 ident: ref7 article-title: Pathogenesis of Hendra and Nipah virus infection in humans publication-title: J Infect Dev Ctries doi: 10.3855/jidc.3648 – volume: 107 start-page: 1062 year: 1995 ident: ref36 article-title: Persistent elevation of inflammatory cytokines predicts a poor outcome in ARDS. Plasma IL-1 beta and IL-6 levels are consistent and efficient predictors of outcome over time publication-title: Chest doi: 10.1378/chest.107.4.1062 – volume: 85 start-page: 7863 year: 2011 ident: ref27 article-title: Nipah virus uses leukocytes for efficient dissemination within a host publication-title: J Virol doi: 10.1128/JVI.00549-11 – volume: 5 start-page: e10690 year: 2010 ident: ref16 article-title: Development of an acute and highly pathogenic nonhuman primate model of nipah virus infection publication-title: PLoS One doi: 10.1371/journal.pone.0010690 – volume: 154 start-page: 180 year: 1995 ident: ref24 article-title: Multiple defects in innate and adaptive immunologic function in NOD/LtSz-scid mice publication-title: J Immunol doi: 10.4049/jimmunol.154.1.180 – volume: 102 start-page: 1014 year: 2009 ident: ref11 article-title: Organ- and endotheliotropism of Nipah virus infections in vivo and in vitro publication-title: Thromb Haemost doi: 10.1160/TH09-05-0310 – volume: 5 start-page: 142 year: 2008 ident: ref10 article-title: Selective receptor expression restricts Nipah virus infection of endothelial cells publication-title: Virol J doi: 10.1186/1743-422X-5-142 – volume: 12 start-page: 1720 year: 2012 ident: ref22 article-title: Human cytomegalovirus infection leads to elevated levels of transplant arteriosclerosis in a humanized mouse aortic xenograft model publication-title: Am J Transplant doi: 10.1111/j.1600-6143.2012.04018.x – volume: 106 start-page: 3455 year: 2009 ident: ref32 article-title: Early and sustained innate immune response defines pathology and death in nonhuman primates infected by highly pathogenic influenza virus publication-title: Proc Natl Acad Sci U S A doi: 10.1073/pnas.0813234106 – volume: 87 start-page: 3284 year: 2013 ident: ref12 article-title: Henipavirus Pathogenesis in Human Respiratory Epithelial Cells publication-title: J Virol doi: 10.1128/JVI.02576-12 – volume: 111 start-page: 1306 year: 1997 ident: ref37 article-title: Infections and the inflammatory response in acute respiratory distress syndrome publication-title: Chest doi: 10.1378/chest.111.5.1306 – volume: 83 start-page: 7062 year: 2009 ident: ref30 article-title: Early upregulation of acute respiratory distress syndrome-associated cytokines promotes lethal disease in an aged-mouse model of severe acute respiratory syndrome coronavirus infection publication-title: J Virol doi: 10.1128/JVI.00127-09 – volume: 354 start-page: 1253 year: 1999 ident: ref3 article-title: Outbreak of Nipah-virus infection among abattoir workers in Singapore publication-title: Lancet doi: 10.1016/S0140-6736(99)04379-2 |
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| Snippet | Nipah virus (NiV) is a member of the genus Henipavirus (family Paramyxoviridae) that causes severe and often lethal respiratory illness and encephalitis in... Nipah virus (NiV) is a member of the genus Henipavirus (family Paramyxoviridae ) that causes severe and often lethal respiratory illness and encephalitis in... Nipah virus (NiV) is a member of the genus Henipavirus (family Paramyxoviridae) that causes severe and often lethal respiratory illness and encephalitis in... |
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| SubjectTerms | Animals Biology and Life Sciences Chemokines Cytokines Cytokines - metabolism Disease Models, Animal Encephalitis Endothelium Epithelial Cells - metabolism Epithelial Cells - pathology Epithelial Cells - virology Health aspects Henipavirus Infections - metabolism Henipavirus Infections - pathology Heterografts Histopathology Host-parasite relationships Host-Pathogen Interactions - physiology Humans Infections Inflammation Ligands Lung Transplantation Lungs Medicine and Health Sciences Mice Mice, Inbred NOD Microbiological research Mortality Nipah virus Nipah Virus - physiology Pathogenesis R&D Research & development Respiratory Mucosa - metabolism Respiratory Mucosa - pathology Respiratory Mucosa - virology Transplants & implants |
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| Title | A Human Lung Xenograft Mouse Model of Nipah Virus Infection |
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