Christopher M. Wiethoff

TL;DR: A new model of Ad entry is proposed based on the present observations of capsid disassembly and membrane penetration, which possessed membrane lytic activity similar to partially disassembled virions.

TL;DR: It is demonstrated that α-synuclein aggregates can induce the rupture of lysosomes following their endocytosis in neuronal cell lines, and Lysosomal rupture is known to induce mitochondrial dysfunction and inflammation, both of which are well established aspects of Parkinson's disease, thus connecting these aspects of Parker's disease to the propagation of α- synuclein pathology in cells.

TL;DR: Using lentivirus-expressed short hairpin RNA (shRNA) and competitive inhibitors, it is shown that Ad-induced IL-1β release is dependent upon Toll-like receptor 9 (TLR9) sensing of the Ad5 double-stranded DNA (dsDNA) genome in human cell lines and primary monocyte-derived macrophage but not in mouse macrophages.

TL;DR: This study found that a PPxY motif within protein VI recruits Nedd4 E3 ubiquitin ligases to bind and ubiquitylate protein VI, providing the first evidence that virus-encoded PPxy motifs are required during virus entry, which may be of significance for several other pathogens.

TL;DR: It is determined that an eight-residue cyclic D,L-α-peptide, selected from a directed combinatorial library, can specifically prevent the development of low pH in endocytic vesicles, arrest the escape of virions from the endosome, and abrogate adenovirus infection without an apparent adverse effect on cell viability.