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  4. Erratum: Distinct Roles of Type i and Type III Interferons in Intestinal Immunity to Homologous and Heterologous Rotavirus Infections (PLoS Pathogens (2016) 12:4 (e1005600) DOI: 10.1371/journal.ppat.1005600)
 
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Erratum: Distinct Roles of Type i and Type III Interferons in Intestinal Immunity to Homologous and Heterologous Rotavirus Infections (PLoS Pathogens (2016) 12:4 (e1005600) DOI: 10.1371/journal.ppat.1005600)

Journal
PLoS Pathogens
Journal Volume
12
Journal Issue
4
Pages
Article number e1005726
Date Issued
2016-06
Author(s)
JIAN-DA LIN  
Feng, Ningguo et al.
DOI
10.1371/journal.ppat.1005726
URI
https://www.scopus.com/inward/record.uri?eid=2-s2.0-84964856244&doi=10.1371%2fjournal.ppat.1005600&partnerID=40&md5=f4cf14cf54de0855b7eaa635b97bab5d
https://scholars.lib.ntu.edu.tw/handle/123456789/612028
Abstract
Type I (IFN-α/β) and type III (IFN-λ) interferons (IFNs) exert shared antiviral activities through distinct receptors. However, their relative importance for antiviral protection of different organ systems against specific viruses remains to be fully explored. We used mouse strains deficient in type-specific IFN signaling, STAT1 and Rag2 to dissect distinct and overlapping contributions of type I and type III IFNs to protection against homologous murine (EW-RV strain) and heterologous (non-murine) simian (RRV strain) rotavirus infections in suckling mice. Experiments demonstrated that murine EW-RV is insensitive to the action of both types of IFNs, and that timely viral clearance depends upon adaptive immune responses. In contrast, both type I and type III IFNs can control replication of the heterologous simian RRV in the gastrointestinal (GI) tract, and they cooperate to limit extra-intestinal simian RRV replication. Surprisingly, intestinal epithelial cells were sensitive to both IFN types in neonatal mice, although their responsiveness to type I, but not type III IFNs, diminished in adult mice, revealing an unexpected age-dependent change in specific contribution of type I versus type III IFNs to antiviral defenses in the GI tract. Transcriptional analysis revealed that intestinal antiviral responses to RV are triggered through either type of IFN receptor, and are greatly diminished when receptors for both IFN types are lacking. These results also demonstrate a murine host-specific resistance to IFN-mediated antiviral effects by murine EW-RV, but the retention of host efficacy through the cooperative action by type I and type III IFNs in restricting heterologous simian RRV growth and systemic replication in suckling mice. Collectively, our findings revealed a well-orchestrated spatial and temporal tuning of innate antiviral responses in the intestinal tract where two types of IFNs through distinct patterns of their expression and distinct but overlapping sets of target cells coordinately regulate antiviral defenses against heterologous or homologous rotaviruses with substantially different effectiveness. © 2016, Public Library of Science. All rights reserved.
SDGs

[SDGs]SDG2

Other Subjects
alpha interferon; beta interferon; gamma interferon; major histocompatibility antigen class 1; STAT1 protein; gamma interferon; interferon; adaptive immunity; adult; animal experiment; animal model; animal tissue; antiviral activity; Article; colorectal cancer cell line; controlled study; enzyme linked immunosorbent assay; flow cytometry; focus forming assay; gene expression; human; human cell; immunohistochemistry; infection control; infectious diarrhea; intestine epithelium cell; intestine infection; mouse; newborn; nonhuman; protein phosphorylation; real time polymerase chain reaction; Rotavirus infection; transcription regulation; viral clearance; virus replication; virus shedding; virus titration; weight gain; Western blotting; animal; C57BL mouse; disease model; immunoblotting; immunology; intestine; knockout mouse; polymerase chain reaction; Rotavirus; Rotavirus infection; Animals; Animals, Newborn; Disease Models, Animal; Enzyme-Linked Immunosorbent Assay; Humans; Immunoblotting; Immunohistochemistry; Interferon Type I; Interferon-gamma; Intestines; Mice; Mice, Inbred C57BL; Mice, Knockout; Polymerase Chain Reaction; Rotavirus; Rotavirus Infections
Publisher
Public Library of Science
Type
corrigendum

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