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Harshad Ingle

Researcher at Washington University in St. Louis

Publications -  17
Citations -  858

Harshad Ingle is an academic researcher from Washington University in St. Louis. The author has contributed to research in topics: Gene & Innate immune system. The author has an hindex of 11, co-authored 17 publications receiving 587 citations. Previous affiliations of Harshad Ingle include Indian Institute of Science Education and Research, Bhopal & Indian Institute of Science.

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Recognition of bacterial infection by innate immune sensors

TL;DR: Recent findings on bacterial recognition by Toll-like receptors and NLRs and the signaling pathways activated by these sensors are reviewed.
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The microRNA miR-485 targets host and influenza virus transcripts to regulate antiviral immunity and restrict viral replication

TL;DR: Inhibition of the expression of mir-485 markedly reduced the replication of Newcastle disease virus and the H5N1 strain of influenza virus in mammalian cells, highlighting the dual role of miR-485 in preventing spurious activation of antiviral signaling and restricting influenza virus infection.
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The interplay between viral-derived miRNAs and host immunity during infection

TL;DR: The origin and biogenesis of viral miRNAs during the viral lifecycle is highlighted and insights into the underexplored role of viralMiRNAs as potential targets for developing therapeutics for treating complex viral diseases are offered.
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Segmented Filamentous Bacteria Prevent and Cure Rotavirus Infection.

TL;DR: It is revealed that segmented filamentous bacteria (SFB) were sufficient to protect mice against RV infection and associated diarrhea, independent of immune cells, and confer protection against certain enteric viral infections and associated diarrheal disease.
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Viral complementation of immunodeficiency confers protection against enteric pathogens via interferon-λ

TL;DR: It is reported that murine astrovirus can complement primary immunodeficiency to protect against murine norovirus and rotavirus infections and that this protection depends on interferon-λ signalling in gut epithelial cells.