DT2 corresponded to anterolateral parts of the SNP and showed an extension to anteromedial part of the CC. The intersections between DT2 and CCP and DT2 and SNP presented both decreased but different T2 values (102 +/- 5 and 95 +/- 4 ms).
An exact differentiation of the SN from the CC is not possible on the basis of T2w images but rather on the basis of the underlying calculated T2 values from
the triple echo sequence.”
“Human cytomegalovirus (HCMV) depends upon a five-protein complex, gH/gL/UL128-131, to enter epithelial and endothelial cells. A separate HCMV gH/gL-containing complex, gH/gL/gO, has been described. Our prevailing model is that gH/gL/UL128-131 selleckchem is required for entry into biologically important epithelial and endothelial cells and that gH/gL/gO is required for infection of fibroblasts. Genes encoding UL128-131 are rapidly mutated during laboratory propagation of HCMV on fibroblasts, apparently related to selective
pressure for the fibroblast entry pathway. Arguing against this model in the accompanying paper by B. J. Ryckman et al. (J. Virol., 84: 2597-2609, 2010), we describe evidence that clinical HCMV strain TR expresses a gO molecule that acts to promote endoplasmic reticulum (ER) export of gH/gL and that gO is not stably incorporated into Z-IETD-FMK order the virus envelope. This was different from results involving fibroblast-adapted HCMV strain AD169, which incorporates gO into the virion envelope. Here, we constructed this website a TR gO-null mutant, TR Delta gO, that replicated to low titers, spread poorly among fibroblasts, but produced normal quantities of extracellular virus particles. TR Delta gO particles released from fibroblasts failed to infect fibroblasts and epithelial and endothelial cells, but the chemical fusogen polyethylene glycol (PEG) could partially overcome defects in infection. Therefore, TR Delta gO is defective for entry into all three cell
types. Defects in entry were explained by observations showing that TR Delta gO incorporated about 5% of the quantities of gH/gL in extracellular virus particles compared with that in wild-type virions. Although TR Delta gO particles could not enter cells, cell-to-cell spread involving epithelial and endothelial cells was increased relative to TR, apparently resulting from increased quantities of gH/gL/UL128-131 in virions. Together, our data suggest that TR gO acts as a chaperone to promote ER export and the incorporation of gH/gL complexes into the HCMV envelope. Moreover, these data suggest that it is gH/gL, and not gH/gL/gO, that is present in virions and is required for infection of fibroblasts and epithelial and endothelial cells. Our observations that both gH/gL and gH/gL/UL128-131 are required for entry into epithelial/endothelial cells differ from models for other beta-and gammaherpesviruses that use one of two different gH/gL complexes to enter different cells.