J
Jason K. Whitmire
Researcher at University of North Carolina at Chapel Hill
Publications - 78
Citations - 6583
Jason K. Whitmire is an academic researcher from University of North Carolina at Chapel Hill. The author has contributed to research in topics: T cell & Cytotoxic T cell. The author has an hindex of 41, co-authored 74 publications receiving 5887 citations. Previous affiliations of Jason K. Whitmire include Oregon Health & Science University & Scripps Research Institute.
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The ZCCHC14/TENT4 complex is required for hepatitis A virus RNA synthesis
You-sheng Li,Ichiro Misumi,Tomoyuki Shiota,Lu Sun,Erik M. Lenarcic,Hyejeong R. Kim,Takayoshi Shirasaki,Adriana Hertel-Wulff,Taylor N. Tibbs,Joseph E. Mitchell,Kevin L. McKnight,Craig E. Cameron,Nathaniel J. Moorman,David R. McGivern,John M. Cullen,Jason K. Whitmire,Stanley M. Lemon +16 more
TL;DR: It is shown that ZCCHC14 and TENT4A/B are required for viral RNA synthesis following translation of the viral genome in infected cells, and suggested that TENT1/B inhibitors may be useful for preventing or treating hepatitis A in humans.
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Iminosugar glucosidase inhibitors reduce hepatic inflammation in HAV-infected Ifnar1-/- mice.
Ichiro Misumi,Zhucui Li,Lu Sun,Anshuman Das,Tomoyuki Shiota,John M. Cullen,Qibin Zhang,Jason K. Whitmire,Stanley M. Lemon +8 more
TL;DR: The authors showed that high doses of the iminosugars miglustat and UV-4 failed to deplete gangliosides sufficiently to block HAV infection in mice lacking a key interferon receptor.
Journal Article
Erratum: CD40 ligand-deficient mice generate a normal primary cytotoxic T-lymphocyte response but a defective humoral response to a viral infection (Journal of Virology 70:12 (8379))
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Editorial: Not all roads to T cell memory go through STAT4 and T-bet.
TL;DR: The early immune response to infection is a carefully orchestrated sequence of events that suppresses early virus replication, while generating adaptive immune responses that not only help to control infection but also form long-lasting immune memory.
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Viral protease cleavage of MAVS in genetically modified mice with hepatitis A virus infection
Lu Sun,Hui Feng,Ichiro Misumi,Takayoshi Shirasaki,Lucinda L. Hensley,Olga González-López,Itoe Shiota,Wei-Chun Chou,Jenny P.-Y. Ting,John M. Cullen,Dale O. Cowley,Jason K. Whitmire,Stanley M. Lemon +12 more
TL;DR: The role of 3ABC protease cleavage in determining hepatitis A virus pathogenesis and host species range was investigated in this article , where the authors showed that 3ABC cleavage of mMAVS enhances HAV replication and lessens liver inflammation in mice lacking interferon receptors, but it is insufficient by itself to overcome the cross-species barrier to infection in mice.