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Book ; Online ; E-Book: Viral gastroenteritis

Svensson, Lennart / Desselberger, Ulrich / Greenberg, Harry B. / Estes, Mary K.

molecular epidemiology and pathogenesis

2016

Author's details	edited by Lennart Svensson, Ulrich Desselberger, Harry B. Greenberg, Mary K. Estes
Keywords	Gastroenteritis / virology ; Gastroenteritis / epidemiology ; RNA Virus Infections / virology ; Rotavirus / pathogenicity ; Norovirus / pathogenicity ; Avastrovirus / pathogenicity
Subject code	616.3/3019
Language	English
Size	1 Online-Ressource (xxvi, 563 Seiten), Illustrationen
Publisher	Elsevier AP
Publishing place	Amsterdam
Publishing country	Netherlands
Document type	Book ; Online ; E-Book
Remark	Zugriff für angemeldete ZB MED-Nutzerinnen und -Nutzer
HBZ-ID	HT019448231
ISBN	978-0-12-802659-5 ; 9780128022412 ; 0-12-802659-6 ; 0128022418
Database	ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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Article ; Online: Organoid Models for Infectious Disease.

Blutt, Sarah E / Estes, Mary K

Annual review of medicine

2021 Volume 73, Page(s) 167–182

Abstract: Infectious diseases affect individual health and have widespread societal impacts. New ex vivo models are critical to understand pathogenesis, host response, and features necessary to develop preventive and therapeutic treatments. Pluripotent and tissue ... ...

Abstract	Infectious diseases affect individual health and have widespread societal impacts. New ex vivo models are critical to understand pathogenesis, host response, and features necessary to develop preventive and therapeutic treatments. Pluripotent and tissue stem cell-derived organoids provide new tools for the study of human infections. Organoid models recapitulate many characteristics of in vivo disease and are providing new insights into human respiratory, gastrointestinal, and neuronal host-microbe interactions. Increasing culture complexity by adding the stroma, interorgan communication, and the microbiome will improve the use of organoids as models for infection. Organoid cultures provide a platform with the capability to improve human health related to infectious diseases.
MeSH term(s)	Communicable Diseases ; Humans ; Organoids
Language	English
Publishing date	2021-10-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	207930-6
ISSN	1545-326X ; 0066-4219
ISSN (online)	1545-326X
ISSN	0066-4219
DOI	10.1146/annurev-med-042320-023055
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Article: Rotavirus-Induced Lipid Droplet Biogenesis Is Critical for Virus Replication.

Criglar, Jeanette M / Estes, Mary K / Crawford, Sue E

Frontiers in physiology

2022 Volume 13, Page(s) 836870

Abstract: A variety of pathogens, including viruses, bacteria and parasites, target cellular lipid droplets for their replication. Rotaviruses (RVs) infect the villous epithelium of the small intestine and are a major cause of acute gastroenteritis in infants and ... ...

Abstract	A variety of pathogens, including viruses, bacteria and parasites, target cellular lipid droplets for their replication. Rotaviruses (RVs) infect the villous epithelium of the small intestine and are a major cause of acute gastroenteritis in infants and young children worldwide. RVs induce and require lipid droplets for the formation of viroplasms, sites of virus genome replication, and nascent particle assembly. Here we review the role of lipid droplets in RV replication. Inhibitors of fatty acid synthesis or chemicals that interfere with lipid droplet homeostasis decrease the number and size of viroplasms and the yield of infectious virus. We used a genetically engineered RV, delayed in viroplasm assembly, to show an early interaction of RV nonstructural protein NSP2 and the lipid droplet-associated protein phospho-PLIN1. The interaction between NSP2 and phospho-PLIN1 suggests that we have identified part of the mechanism of RV-induced lipid droplet formation. These studies demonstrate that RV is an excellent model to dissect the cellular process of lipid droplet formation and to determine how RV induces and usurps lipid droplet biogenesis to form viroplasm/lipid droplets for virus replication.
Language	English
Publishing date	2022-03-23
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2564217-0
ISSN	1664-042X
ISSN	1664-042X
DOI	10.3389/fphys.2022.836870
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Article ; Online: Generation of CRISPR-Cas9-mediated genetic knockout human intestinal tissue-derived enteroid lines by lentivirus transduction and single-cell cloning.

Lin, Shih-Ching / Haga, Kei / Zeng, Xi-Lei / Estes, Mary K

Nature protocols

2022 Volume 17, Issue 4, Page(s) 1004–1027

Abstract: Human intestinal tissue-derived enteroids (HIEs; also called organoids) are a powerful ex vivo model for gastrointestinal research. Genetic modification of these nontransformed cultures allows new insights into gene function and biological processes ... ...

Abstract	Human intestinal tissue-derived enteroids (HIEs; also called organoids) are a powerful ex vivo model for gastrointestinal research. Genetic modification of these nontransformed cultures allows new insights into gene function and biological processes involved in intestinal diseases as well as gastrointestinal and donor segment-specific function. Here we provide a detailed technical pipeline and protocol for using the CRISPR-Cas9 genome editing system to knock out a gene of interest specifically in HIEs by lentiviral transduction and single-cell cloning. This protocol differs from a previously published alternative using electroporation of human colonoids to deliver piggyback transposons or CRISPR-Cas9 constructs, as this protocol uses a modified, fused LentiCRISPRv2-small-guiding RNA to express Cas9 and small-guiding RNA in a lentivirus. The protocol also includes the steps of gene delivery and subsequent single-cell cloning of the knockout cells as well as verification of clones and sequence identification of the mutation sites to establish knockout clones. An overview flowchart, step-by-step guidelines and troubleshooting suggestions are provided to aid the researcher in obtaining the genetic knockout HIE line within 2-3 months. In this protocol, we further describe how to use HIEs as an ex vivo model to assess host restriction factors for viral replication (using human norovirus replication as an example) by knocking out host attachment factors or innate immunity genes. Other applications are discussed to broaden the utility of this system, for example, to generate knockin or conditional knockout HIE lines to investigate the function of essential genes in many biological processes including other types of organoids.
MeSH term(s)	CRISPR-Cas Systems/genetics ; Clone Cells ; Cloning, Molecular ; Gene Editing/methods ; Gene Knockout Techniques ; Humans ; Lentivirus/genetics ; RNA, Guide, CRISPR-Cas Systems/genetics
Chemical Substances	RNA, Guide, CRISPR-Cas Systems
Language	English
Publishing date	2022-02-23
Publishing country	England
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2244966-8
ISSN	1750-2799 ; 1754-2189
ISSN (online)	1750-2799
ISSN	1754-2189
DOI	10.1038/s41596-021-00669-0
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Article ; Online: Mapping human norovirus antigens during infection reveals the breadth of the humoral immune response.

Su, Lynn / Huang, Wanzhi / Neill, Frederick H / Estes, Mary K / Atmar, Robert L / Palzkill, Timothy

NPJ vaccines

2023 Volume 8, Issue 1, Page(s) 87

Abstract: Human noroviruses (HuNoV) are the leading cause of acute gastroenteritis worldwide. The humoral immune response plays an important role in clearing HuNoV infections and elucidating the antigenic landscape of HuNoV during an infection can shed light on ... ...

Abstract	Human noroviruses (HuNoV) are the leading cause of acute gastroenteritis worldwide. The humoral immune response plays an important role in clearing HuNoV infections and elucidating the antigenic landscape of HuNoV during an infection can shed light on antibody targets to inform vaccine design. Here, we utilized Jun-Fos-assisted phage display of a HuNoV genogroup GI.1 genomic library and deep sequencing to simultaneously map the epitopes of serum antibodies of six individuals infected with GI.1 HuNoV. We found both unique and common epitopes that were widely distributed among both nonstructural proteins and the major capsid protein. Recurring epitope profiles suggest immunodominant antibody footprints among these individuals. Analysis of sera collected longitudinally from three individuals showed the presence of existing epitopes in the pre-infection sera, suggesting these individuals had prior HuNoV infections. Nevertheless, newly recognized epitopes surfaced seven days post-infection. These new epitope signals persisted by 180 days post-infection along with the pre-infection epitopes, suggesting a persistent production of antibodies recognizing epitopes from previous and new infections. Lastly, analysis of a GII.4 genotype genomic phage display library with sera of three persons infected with GII.4 virus revealed epitopes that overlapped with those identified in GI.1 affinity selections, suggesting the presence of GI.1/GII.4 cross-reactive antibodies. The results demonstrate that genomic phage display coupled with deep sequencing can characterize HuNoV antigenic landscapes from complex polyclonal human sera to reveal the timing and breadth of the human humoral immune response to infection.
Language	English
Publishing date	2023-06-06
Publishing country	England
Document type	Journal Article
ISSN	2059-0105
ISSN (online)	2059-0105
DOI	10.1038/s41541-023-00683-1
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Article: Bile acid-sensitive human norovirus strains are susceptible to sphingosine-1-phosphate receptor 2 inhibition.

Tenge, Victoria / Vijayalakshmi Ayyar, B / Ettayebi, Khalil / Crawford, Sue E / Shen, Yi-Ting / Neill, Frederick H / Atmar, Robert L / Estes, Mary K

bioRxiv : the preprint server for biology

2024

Abstract: Human noroviruses (HuNoVs) are a diverse group of RNA viruses that cause both endemic and pandemic acute viral gastroenteritis. Previously we reported that many strains of HuNoV require bile or bile acid (BA) to infect human jejunal intestinal enteroid ... ...

Abstract	Human noroviruses (HuNoVs) are a diverse group of RNA viruses that cause both endemic and pandemic acute viral gastroenteritis. Previously we reported that many strains of HuNoV require bile or bile acid (BA) to infect human jejunal intestinal enteroid cultures. Of note, BA was not essential for replication of a pandemic-causing GII.4 HuNoV strain. Using the BA-requiring strain GII.3, we found that the hydrophobic BA GCDCA induces multiple cellular responses that promote replication in jejunal enteroids. Further, we found that chemical inhibition of the G-protein coupled receptor, sphingosine-1- phosphate receptor 2 (S1PR2), by JTE-013 reduced both GII.3 infection in a dose- dependent manner and cellular uptake in enteroids. Herein, we sought to determine if S1PR2 is required by other BA-dependent HuNoV strains and BA-independent GII.4, and if S1PR2 is required for BA-dependent HuNoV infection in other segments of the small intestine. We found JTE-013 inhibition of S1PR2 in jejunal HIEs reduces GI.1, GII.3, and GII.17 (BA-dependent) but not the GII.4 Sydney variant (BA-independent) infection, providing additional evidence of strain-specific differences in HuNoV infection. GII.3 infection of duodenal, jejunal and ileal lines derived from the same individual was also reduced with S1PR2 inhibition, indicating a common mechanism of BA-dependent infection among multiple segments of the small intestine. Our results support a model where BA-dependent HuNoV exploit the activation of S1PR2 by BA to infect the entire small intestine. Importance: Human noroviruses (HuNoVs) are important viral human pathogens that cause both outbreaks and sporadic gastroenteritis. These viruses are diverse, and many strains are capable of infecting humans. Our previous studies have identified strain-specific requirements for hydrophobic bile acids (BAs) to infect intestinal epithelial cells. Moreover, we identified a BA receptor, sphingosine-1-phosphate receptor 2 (S1PR2), required for infection by a BA-dependent strain. To better understand how various HuNoV strains enter and infect the small intestine and the role of S1PR2 in HuNoV infection, we evaluated infection by additional HuNoV strains using an expanded repertoire of intestinal enteroid cell lines. We found that multiple BA-dependent strains, but not a BA- independent strain, all required S1PR2 for infection. Additionally, BA-dependent infection required S1PR2 in multiple segments of the small intestine. Together these results indicate S1PR2 has value as a potential therapeutic target for BA-dependent HuNoV infection.
Language	English
Publishing date	2024-01-03
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.01.02.573926
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Article ; Online: Gut Bacterial Bouncers: Keeping Viral Pathogens out of the Epithelium.

Blutt, Sarah E / Estes, Mary K

Cell host & microbe

2019 Volume 26, Issue 5, Page(s) 569–570

Abstract: Intestinal pathogens encounter the microbiota as they seek their host target, potentially impacting the infection. In a recent Cell paper, Shi et al. (2019) show that unique segmented filamentous bacteria prevent rotavirus from infecting the intestinal ... ...

Abstract	Intestinal pathogens encounter the microbiota as they seek their host target, potentially impacting the infection. In a recent Cell paper, Shi et al. (2019) show that unique segmented filamentous bacteria prevent rotavirus from infecting the intestinal epithelium. Proposed mechanisms include direct effects on the virus and stimulation of epithelial proliferation.
MeSH term(s)	Bacteria ; Gastrointestinal Microbiome ; Humans ; Intestinal Mucosa ; Intestines ; Rotavirus Infections
Language	English
Publishing date	2019-11-21
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	2278004-X
ISSN	1934-6069 ; 1931-3128
ISSN (online)	1934-6069
ISSN	1931-3128
DOI	10.1016/j.chom.2019.10.018
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Article ; Online: N-glycoproteomic analyses of human intestinal enteroids, varying in histo-blood group geno- and phenotypes, reveal a wide repertoire of fucosylated glycoproteins.

Nilsson, Jonas / Rimkute, Inga / Sihlbom, Carina / Tenge, Victoria R / Lin, Shih-Ching / Atmar, Robert L / Estes, Mary K / Larson, Göran

Glycobiology

2024 Volume 34, Issue 6

Abstract: Human noroviruses, globally the main cause of viral gastroenteritis, show strain specific affinity for histo-blood group antigens (HBGA) and can successfully be propagated ex vivo in human intestinal enteroids (HIEs). HIEs established from jejunal stem ... ...

Abstract	Human noroviruses, globally the main cause of viral gastroenteritis, show strain specific affinity for histo-blood group antigens (HBGA) and can successfully be propagated ex vivo in human intestinal enteroids (HIEs). HIEs established from jejunal stem cells of individuals with different ABO, Lewis and secretor geno- and phenotypes, show varying susceptibility to such infections. Using bottom-up glycoproteomic approaches we have defined and compared the N-linked glycans of glycoproteins of seven jejunal HIEs. Membrane proteins were extracted, trypsin digested, and glycopeptides enriched by hydrophilic interaction liquid chromatography and analyzed by nanoLC-MS/MS. The Byonic software was used for glycopeptide identification followed by hands-on verifications and interpretations. Glycan structures and attachment sites were identified from MS2 spectra obtained by higher-energy collision dissociation through analysis of diagnostic saccharide oxonium ions (B-ions), stepwise glycosidic fragmentation of the glycans (Y-ions), and peptide sequence ions (b- and y-ions). Altogether 694 unique glycopeptides from 93 glycoproteins were identified. The N-glycans encompassed pauci- and oligomannose, hybrid- and complex-type structures. Notably, polyfucosylated HBGA-containing glycopeptides of the four glycoproteins tetraspanin-8, carcinoembryonic antigen-related cell adhesion molecule 5, sucrose-isomaltase and aminopeptidase N were especially prominent and were characterized in detail and related to donor ABO, Lewis and secretor types of each HIE. Virtually no sialylated N-glycans were identified for these glycoproteins suggesting that terminal sialylation was infrequent compared to fucosylation and HBGA biosynthesis. This approach gives unique site-specific information on the structural complexity of N-linked glycans of glycoproteins of human HIEs and provides a platform for future studies on the role of host glycoproteins in gastrointestinal infectious diseases.
MeSH term(s)	Humans ; Glycoproteins/metabolism ; Glycoproteins/chemistry ; Proteomics/methods ; Blood Group Antigens/metabolism ; Blood Group Antigens/chemistry ; Polysaccharides/chemistry ; Polysaccharides/metabolism ; Fucose/metabolism ; Fucose/chemistry ; Phenotype ; Glycosylation ; ABO Blood-Group System/metabolism ; ABO Blood-Group System/chemistry
Chemical Substances	Glycoproteins ; Blood Group Antigens ; Polysaccharides ; Fucose (28RYY2IV3F) ; ABO Blood-Group System
Language	English
Publishing date	2024-04-08
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1067689-2
ISSN	1460-2423 ; 0959-6658
ISSN (online)	1460-2423
ISSN	0959-6658
DOI	10.1093/glycob/cwae029
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Article ; Online: Plasmid-based reverse genetics for probing phosphorylation-dependent viroplasm formation in rotaviruses.

Criglar, Jeanette M / Crawford, Sue E / Estes, Mary K

Virus research

2020 Volume 291, Page(s) 198193

Abstract: Rotavirus (RV) replication occurs in cytoplasmic compartments, known as viroplasms, that are composed of viral and cellular proteins. Viroplasm formation requires RV nonstructural proteins NSP2 and NSP5 and cellular lipid droplets (LDs); however, the ... ...

Abstract	Rotavirus (RV) replication occurs in cytoplasmic compartments, known as viroplasms, that are composed of viral and cellular proteins. Viroplasm formation requires RV nonstructural proteins NSP2 and NSP5 and cellular lipid droplets (LDs); however, the mechanisms required for viroplasm assembly remain largely unknown. We previously identified two conformationally-distinct forms of NSP2 (dNSP2, vNSP2) found in RV-infected cells that interact differentially with hypo- and hyperphosphorylated NSP5, respectively, and indicate a coordinated phosphorylation-dependent mechanism regulating viroplasm assembly. We also reported that phosphorylation of dNSP2 on serine 313 by the cellular kinase CK1α triggers the localization of vNSP2 to sites of viroplasm assembly and its association with hyperphosphorylated NSP5. To directly evaluate the role of CK1α-mediated NSP2 phosphorylation on viroplasm formation, we used a recently published plasmid-based reverse genetics method to generate a recombinant rotavirus (rRV) with a phosphomimetic NSP2 mutation (rRV NSP2 S313D). The rRV NSP2 S313D virus is significantly delayed in viroplasm formation, virus replication, and interferes with wild type RV replication during co-infection. The rRV NSP2 S313A virus was not rescued. Taking advantage of the delay in viroplasm formation, the NSP2 S313D phosphomimetic mutant was used as a tool to observe very early events in viroplasm assembly. We show that (1) viroplasm assembly correlates with NSP5 hyperphosphorylation, and (2) that vNSP2 S313D co-localizes with RV-induced LDs without NSP5, suggesting that vNSP2 phospho-S313 is sufficient for interacting with LDs and may be the virus factor required for RV-induced LD formation. Further studies with the rRV NSP2 S313D virus are expected to reveal new aspects of viroplasm and LD initiation and assembly.
MeSH term(s)	Cytoplasm/virology ; Humans ; Phosphorylation ; Plasmids/genetics ; Reverse Genetics/methods ; Rotavirus/genetics ; Rotavirus/physiology ; Rotavirus Infections/virology ; Virus Replication
Language	English
Publishing date	2020-10-11
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	605780-9
ISSN	1872-7492 ; 0168-1702
ISSN (online)	1872-7492
ISSN	0168-1702
DOI	10.1016/j.virusres.2020.198193
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Zs.A 1965: Show issues

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Article ; Online: Organoids to Dissect Gastrointestinal Virus-Host Interactions: What Have We Learned?

Crawford, Sue E / Ramani, Sasirekha / Blutt, Sarah E / Estes, Mary K

Viruses

2021 Volume 13, Issue 6

Abstract: Historically, knowledge of human host-enteric pathogen interactions has been elucidated from studies using cancer cells, animal models, clinical data, and occasionally, controlled human infection models. Although much has been learned from these studies, ...

Abstract	Historically, knowledge of human host-enteric pathogen interactions has been elucidated from studies using cancer cells, animal models, clinical data, and occasionally, controlled human infection models. Although much has been learned from these studies, an understanding of the complex interactions between human viruses and the human intestinal epithelium was initially limited by the lack of nontransformed culture systems, which recapitulate the relevant heterogenous cell types that comprise the intestinal villus epithelium. New investigations using multicellular, physiologically active, organotypic cultures produced from intestinal stem cells isolated from biopsies or surgical specimens provide an exciting new avenue for understanding human specific pathogens and revealing previously unknown host-microbe interactions that affect replication and outcomes of human infections. Here, we summarize recent biologic discoveries using human intestinal organoids and human enteric viral pathogens.
MeSH term(s)	Cell Culture Techniques/methods ; Gastrointestinal Diseases/virology ; Gastrointestinal Tract/virology ; Host-Pathogen Interactions ; Humans ; Organoids/virology ; Stem Cells ; Viruses/genetics ; Viruses/pathogenicity
Language	English
Publishing date	2021-05-27
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2516098-9
ISSN	1999-4915 ; 1999-4915
ISSN (online)	1999-4915
ISSN	1999-4915
DOI	10.3390/v13060999
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