Joseph E. Mitchell

ORCID: 0000-0001-9617-0044
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About
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Research Areas
  • Hepatitis B Virus Studies
  • Hepatitis Viruses Studies and Epidemiology
  • Hepatitis C virus research
  • T-cell and B-cell Immunology
  • Immune Cell Function and Interaction
  • Erythrocyte Function and Pathophysiology
  • Viral Infections and Vectors
  • Immunotherapy and Immune Responses
  • Viral Infections and Outbreaks Research
  • Viral Infections and Immunology Research
  • Inflammasome and immune disorders
  • Cell death mechanisms and regulation

University of North Carolina at Chapel Hill
2019-2022

Despite excellent vaccines, resurgent outbreaks of hepatitis A have caused thousands hospitalizations and hundreds deaths within the United States in recent years. There is no effective antiviral therapy for A, many aspects virus (HAV) replication cycle remain to be elucidated. Replication requires zinc finger protein ZCCHC14 noncanonical TENT4 poly(A) polymerases with which it associates, but underlying mechanism unknown. Here, we show that TENT4A/B are required viral RNA synthesis...

10.1073/pnas.2204511119 article EN cc-by-nc-nd Proceedings of the National Academy of Sciences 2022-07-07

•T cells protect against HAV-mediated liver injury and can be targeted to improve health.•Ifnar1-/- mice are permissive for HAV generate HAV-specific T within the during infection.•HAV replication was enhanced disease exacerbated when were depleted of CD4+ or CD8+ cells.•Peptide vaccination increased virus-specific cell frequencies reduced viral RNA injury. Background & AimsHepatitis A virus (HAV) is a common cause enterically transmitted hepatitis. In non-immune individuals, infection...

10.1016/j.jhep.2021.07.019 article EN cc-by-nc-nd Journal of Hepatology 2021-07-29

Persistent virus infections can cause pathogenesis that is debilitating or lethal. During these infections, virus-specific T cells fail to protect due weakened antiviral activity failure persist. These outcomes are governed by histone modifications, although it unknown which enzymes contribute cell loss impaired function over time. In this study, we show receptor-stimulated CD8+ increase their expression of UTX (ubiquitously transcribed tetratricopeptide repeat, X chromosome) enhance gene...

10.1016/j.celrep.2021.108966 article EN cc-by-nc-nd Cell Reports 2021-04-01

Arenaviruses can cause severe hemorrhagic disease in humans, which progress to organ failure and death. The underlying mechanisms causing lethality person-to-person variation outcome remain incompletely explained. Herein, we characterize a mouse model that recapitulates many features of pathogenesis observed humans with arenavirus-induced disease, including thrombocytopenia, vascular leakage, lung edema, lethality. susceptibility congenic B6.PL mice lymphocytic choriomeningitis virus (LCMV)...

10.1016/j.celrep.2019.04.004 article EN cc-by-nc-nd Cell Reports 2019-04-01
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