Mitchell Hayes
University of Wisconsin-Madison
17 Papers
5 Citations
Mitchell Hayes is an academic researcher from University of Wisconsin-Madison. The author has contributed to research in topics: Epstein–Barr virus & Biology. The author has an hindex of 8, co-authored 12 publications.
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Papers
A cancer-associated Epstein-Barr virus BZLF1 promoter variant enhances lytic infection.
Jillian A. Bristol,Reza Djavadian,Emily R. Albright,Carrie B. Coleman,Makoto Ohashi,Mitchell Hayes,James C. Romero-Masters,Elizabeth A. Barlow,Paul J. Farrell,Rosemary Rochford,Rosemary Rochford,Robert F. Kalejta,Eric Johannsen,Shannon C. Kenney +13 more
TL;DR: It is demonstrated that the Zp-V3 enhances EBV lytic reactivation to physiologically-relevant stimuli, and suggested that increased lytic infection may contribute to the increased prevalence of this variant in EBV-associated malignancies.
CAGE-seq analysis of Epstein-Barr virus lytic gene transcription: 3 kinetic classes from 2 mechanisms.
TL;DR: This work identifies 16 true-late, 32 early, and 16 TSS that are active at low levels early and are further upregulated in a DNA replication-dependent manner (leaky late), and suggests that most, but not all EBV late genes are vPIC-dependent.
Multiple functions are mediated by the miRNAs of Epstein-Barr virus.
TL;DR: This work shall summarize these targets, the robustness of their identification, and examine how the regulation of these targets by EBV contributes to the successful infection of its host.
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EBNA2-deleted Epstein-Barr virus (EBV) isolate, P3HR1, causes Hodgkin-like lymphomas and diffuse large B cell lymphomas with type II and Wp-restricted latency types in humanized mice
Chunrong Li,James C. Romero-Masters,Shane M. Huebner,Makoto Ohashi,Mitchell Hayes,Jillian A. Bristol,Scott E. Nelson,Mark R. Eichelberg,Nicholas Van Sciver,Erik A. Ranheim,Rona S. Scott,Eric Johannsen,Shannon C. Kenney +12 more
TL;DR: It is shown that a naturally occurring EBNA2-deleted EBV strain (P3HR1) isolated from a human BL induces EBV-positive B-cell lymphomas in a subset of infected cord blood-humanized (CBH) mice and suggests that P3 HR1 virus can be used to model EBV positive lymphomas with both Wp-restricted and type II latency in vivo.
An EBNA3C-deleted Epstein-Barr virus (EBV) mutant causes B-cell lymphomas with delayed onset in a cord blood-humanized mouse model.
James C. Romero-Masters,Makoto Ohashi,Reza Djavadian,Mark R. Eichelberg,Mitchell Hayes,Jillian A. Bristol,Shidong Ma,Erik A. Ranheim,Jenny E. Gumperz,Eric Johannsen,Shannon C. Kenney +10 more
TL;DR: The phenotype of an EBNAC-deleted virus (Δ3C EBV) in a cord blood-humanized mouse model (CBH) is examined, revealing that EBNA3C contributes to, but is not essential for, EBV-induced lymphomagenesis in CBH mice, and suggest potentially important immunologic roles of EBNA2C in vivo.