H
Haitao Guo
Researcher at University of North Carolina at Chapel Hill
Publications - 24
Citations - 4000
Haitao Guo is an academic researcher from University of North Carolina at Chapel Hill. The author has contributed to research in topics: Innate immune system & Viral replication. The author has an hindex of 15, co-authored 24 publications receiving 2942 citations. Previous affiliations of Haitao Guo include Chinese Academy of Sciences.
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Journal ArticleDOI
Inflammasomes: mechanism of action, role in disease, and therapeutics
TL;DR: Increasing evidence in mouse models strongly implicates an involvement of the inflammasome in the initiation or progression of diseases with a high impact on public health, such as metabolic disorders and neurodegenerative diseases.
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Interferon-inducible cholesterol-25-hydroxylase broadly inhibits viral entry by production of 25-hydroxycholesterol.
Su-Yang Liu,Roghiyh Aliyari,Kelechi Chikere,Guangming Li,Matthew D. Marsden,Jennifer K. Smith,Olivier Pernet,Haitao Guo,Rebecca J. Nusbaum,Jerome A. Zack,Alexander N. Freiberg,Lishan Su,Benhur Lee,Genhong Cheng +13 more
TL;DR: The studies demonstrate a unique mechanism by which IFN achieves its antiviral state through the production of a natural oxysterol to inhibit viral entry and implicate membrane-modifying oxysterols as potential antiviral therapeutics.
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NLR members NLRC4 and NLRP3 mediate sterile inflammasome activation in microglia and astrocytes.
Leslie Freeman,Haitao Guo,Clément N. David,W. June Brickey,Sushmita Jha,Sushmita Jha,Jenny P.-Y. Ting +6 more
TL;DR: It is revealed that lysophosphatidylcholine (LPC), a molecule associated with neurodegeneration and demyelination, elicits NLRP3 and NLRC4 inflammasome activation in microglia and astrocytes, which are central players in neuroinflammation.
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HIV-1 infection induces interleukin-1β production via TLR8 protein-dependent and NLRP3 inflammasome mechanisms in human monocytes.
TL;DR: HIV-1 infection in human monocytes efficiently induced the expression of pro-IL-1β via TLR8-mediated mechanisms and activated caspase-1 through the NLRP3 inflammasome to cleave pro- IL- 1β into bioactive IL-1 β.
Journal ArticleDOI
NLRX1 Sequesters STING to Negatively Regulate the Interferon Response, Thereby Facilitating the Replication of HIV-1 and DNA Viruses
Haitao Guo,Renate König,Renate König,Meng Deng,Maximilian Riess,Jinyao Mo,Lu Zhang,Alex Petrucelli,Sunnie M. Yoh,Brice E. Barefoot,Melissa Samo,Gregory D. Sempowski,Aiping Zhang,Anamaris M. Colberg-Poley,Anamaris M. Colberg-Poley,Hui Feng,Stanley M. Lemon,Yong Liu,Yanping Zhang,Haitao Wen,Zhigang Zhang,Blossom Damania,Li-Chung Tsao,Qi Wang,Lishan Su,Joseph A. Duncan,Sumit K. Chanda,Jenny P.-Y. Ting +27 more
TL;DR: Nlrx1(-/-) mice infected with DNA viruses exhibit enhanced innate immunity and reduced viral load and NLRX1 is a negative regulator of the host innate immune response to HIV-1 and DNA viruses.