12 research outputs found
A Model for the Development of a Reading and Study Skills Inventory for Every Content Area
No full textSequential injection analysis coupled to on-line benchtop proton NMR: Method development and application to the determination of synthetic cathinones in seized drug samples
No full text
From ADAM to SAM: Academic Diagnostic Motivation Service to Student Academic Motivation Center
No full textGammaherpesvirus entry and fusion: A tale how two human pathogenic viruses enter their host cells.
No full textThe prototypical human.-herpesviruses Epstein-Barr virus (EBV) and Kaposi Sarcoma-associated herpesvirus (KSHV) are involved in the development of malignancies. Like all herpesviruses, they share the establishment of latency, the typical architecture, and the conserved fusion machinery to initiate infection. The fusion machinery reflects virus-specific adaptations due to the requirements of the respective herpesvirus. For example, EBV evolved a tropism switch involving either the B-or epithelial cell-tropism complexes to activate fusion driven by gB. Most of the EBV entry proteins and their cellular receptors have been crystallized providing molecular details of the initial steps of infection. For KSHV, a variety of entry and binding receptors has also been reported but the mechanism how receptor binding activates gB-driven fusion is not as well understood as that for EBV. However, the downstream signaling pathways that promote the early steps of KSHV entry are well described. This review summarizes the current knowledge of the key players involved in EBV and KSHV entry and the cell-type specific mechanisms that allow infection of a wide variety of cell types
