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William T. Jackson
Researcher at University of Maryland, Baltimore
Publications - 50
Citations - 16134
William T. Jackson is an academic researcher from University of Maryland, Baltimore. The author has contributed to research in topics: Autophagy & Viral replication. The author has an hindex of 26, co-authored 45 publications receiving 13499 citations. Previous affiliations of William T. Jackson include Stanford University & Medical College of Wisconsin.
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Complexity and ultrastructure of infectious extracellular vesicles from cells infected by non-enveloped virus
Jie E. Yang,Evan Rossignol,Deborah Chang,Joseph Zaia,Isaac Forrester,Holly M. Saulsbery,Daniela Nicastro,William T. Jackson,Esther Bullitt +8 more
TL;DR: The data show that, prior to cell lysis, non-enveloped viruses are secreted within infectious vesicles that also transport viral and host RNAs and proteins, as well as cellular resources from the host.
Journal ArticleDOI
Dangerous Membranes: Viruses That Subvert Autophagosomes.
TL;DR: In this issue of EBioMedicine, Christian Munz and colleagues show that Epstein–Barr Virus (EBV) induces an accumulation of membranes related to the cellular autophagy pathway, and that an autophagic marker can be found in EBV particles (Nowag et al., 2014), which suggests thatAutophagic membranes participate in generation of the viral envelope.
Journal ArticleDOI
Starvation after infection restricts enterovirus D68 replication
Alagie Jassey,Michael A. Wagner,Ganna Galitska,Bimala Devi Paudel,Katelyn D. Miller,William T. Jackson +5 more
TL;DR: SAI, but not SBI, attenuated EV-D68 replication in multiple cell lines and abrogated the viral-mediated cleavage of host autophagic flux-related proteins, which identified SAI as an attractive broad-spectrum anti-picornavirus strategy.
BookDOI
Autophagy, Infection, and the Immune Response
TL;DR: Autophagy, Infection, and the Immune Response provides a unified overview of the roles of cellular autophagy during microbial infection and to systemic immune responses, including antigen presentation, ER stress, and production of IFN-gamma.
Journal ArticleDOI
SNAP23 is essential for germination of EV-D68 replication organelles.
TL;DR: In this paper , the Qbc SNARE, SNAP23, is found at the plasma membrane and plays roles in exocytosis, and it is found that knockdown of SNAP23 expression inhibits virus replication but not release from cells.