John Sinclair

TL;DR: This systematic analysis of the massive transcriptome RNA sequencing atlas generated by the Genotype-Tissue Expression project reveals that HCMV persistence in vivo is prevalent in diverse tissues and suggests that latency is governed mainly by quantitative changes, with a limited number of qualitative changes, in viral gene expression.

TL;DR: In monocytes, which are recognized sites of HCMV latency in vivo, US28 attenuates multiple cell signaling pathways, and that this is required to establish a latent infection; viruses deleted for US28 initiate a lytic infection in infected monocytes are shown.

TL;DR: It is shown that the expression of US28 on the surface of latently infected cells allows monocytes and their progenitor CD34+ cells to be targeted and killed by F49A-FTP, a highly specific fusion toxin protein that binds this viral GPCR.

TL;DR: It is validated that major histocompatibility complex (MHC) class II and two pyrin and HIN domain (PYHIN) proteins, myeloid cell nuclear differentiation antigen (MNDA) and IFI16, are downregulated during experimental latency in primary human CD14+ monocytes, and it is found that IFI 16 is targeted rapidly during the establishment of latency in a US28-dependent manner but only in undifferentiated myeloids cells, a

TL;DR: This systematic analysis reveals that HCMV persistence in-vivo is prevalent in diverse tissues and suggests that latency is governed by quantitative but not qualitative changes in viral gene expression.