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Replication of Norovirus in Cell Culture Reveals a Tropism for Dendritic Cells and Macrophages

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TLDR
The capacity of MNV-1 to replicate in a STAT-1-regulated fashion and the unexpected tropism of a norovirus for cells of the hematopoietic lineage provide important insights into Norovirus biology.
Abstract
Noroviruses are understudied because these important enteric pathogens have not been cultured to date. We found that the norovirus murine norovirus 1 (MNV-1) infects macrophage-like cells in vivo and replicates in cultured primary dendritic cells and macrophages. MNV-1 growth was inhibited by the interferon-alphabeta receptor and STAT-1, and was associated with extensive rearrangements of intracellular membranes. An amino acid substitution in the capsid protein of serially passaged MNV-1 was associated with virulence attenuation in vivo. This is the first report of replication of a norovirus in cell culture. The capacity of MNV-1 to replicate in a STAT-1-regulated fashion and the unexpected tropism of a norovirus for cells of the hematopoietic lineage provide important insights into norovirus biology.

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Journal ArticleDOI

Norovirus classification and proposed strain nomenclature

TL;DR: Analyses of the pairwise distances demonstrated three clearly resolved peaks, suggesting that NoV strains beneath the species level can be classified at three levels: strain (S), cluster (C), and genogroup (G).
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Droplet microfluidics for high-throughput biological assays

TL;DR: Droplets allow sample volumes to be significantly reduced, leading to concomitant reductions in cost, and compartmentalization in droplets increases assay sensitivity by increasing the effective concentration of rare species and decreasing the time required to reach detection thresholds.
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Cross-Species Virus Transmission and the Emergence of New Epidemic Diseases

TL;DR: What is known about host switching leading to viral emergence from known examples is reviewed, considering the evolutionary mechanisms, virus-host interactions, host range barriers to infection, and processes that allow efficient host-to-host transmission in the new host population.
Journal ArticleDOI

Enteric bacteria promote human and mouse norovirus infection of B cells.

TL;DR: B cells are identified as a cellular target of noroviruses and enteric bacteria as a stimulatory factor for norovirus infection, leading to the development of an in vitro infection model for human norovIRuses.
Journal ArticleDOI

Murine Norovirus: a Model System To Study Norovirus Biology and Pathogenesis

TL;DR: This chapter discusses human noroviruses, which are the major cause of nonbacterial, epidemic gastroenteritis worldwide and cause significant numbers of endemic cases, as well as investigating the mechanisms behind their spread.
References
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Book

Molecular Cloning: A Laboratory Manual

TL;DR: Molecular Cloning has served as the foundation of technical expertise in labs worldwide for 30 years as mentioned in this paper and has been so popular, or so influential, that no other manual has been more widely used and influential.
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Functional role of type I and type II interferons in antiviral defense.

TL;DR: Comparison of mice lacking either type I or type II IFN receptors showed that, at least in response to some viruses, both IFN systems are essential for antiviral defense and are functionally nonredundant.
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Targeted Disruption of the Mouse Stat1 Gene Results in Compromised Innate Immunity to Viral Disease

TL;DR: Cell and tissues from Stat1(-1-1) mice were unresponsive to IFN, but remained responsive to all other cytokines tested, indicating that STAT1 appears to be specific for IFN pathways that are essential for viability in the face of otherwise innocuous pathogens.
Journal ArticleDOI

Altered responses to bacterial infection and endotoxic shock in mice lacking inducible nitric oxide synthase

TL;DR: Mice deficient in inducible nitric oxide synthase (iNOS) were generated to test the idea that iNOS defends the host against infectious agents and tumor cells at the risk of contributing to tissue damage and shock, and found there exist both iN OS-dependent and iNos-independent routes to LPS-induced hypotension and death.
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