Vu Thuy Khanh Le

TL;DR: The results reveal an unanticipated complexity to the HCMV coding capacity and illustrate the role of regulated changes in transcript start sites in generating this complexity.

TL;DR: Together, the results reveal that IL-12, CD14(+) cells, and the CD94/NKG2C/HLA-E axis are critical for the expansion of NKG 2C(+) NK cells in response to HCMV infection.

TL;DR: This work has identified the latency-associated gene product pUL138, which also is expressed during productive infection, as a selective potentiator of tumor necrosis factor receptor 1, one of the key receptors of innate immunity, and identifies this region as a hub for multilayered tumor Necrosis factor alpha signaling regulation.

TL;DR: HCMV abrogates IFN receptor signalling at multiple checkpoints by independent mechanisms including UL27-independent degradation of STAT2 and a preceding blockade ofstat2 phosphorylation, suggesting degradation ofSTAT2 via the ubiquitin proteasome pathway.

TL;DR: Surface immune-precipitation showed that both HCMV-encoded Fcγ binding proteins have the capacity to bind trastuzumab antibody-HER2 antigen complexes demonstrating simultaneous linkage of immune IgG with antigen and the H CMV inhibitors on the plasma membrane.