Quantitative temporal viromics: an approach to investigate host-pathogen interaction.
Bottom Line: QTV predicted natural killer and T cell ligands, as well as 29 viral proteins present at the cell surface, potential therapeutic targets.Temporal profiles of >80% of HCMV canonical genes and 14 noncanonical HCMV open reading frames were defined.QTV is a powerful method that can yield important insights into viral infection and is applicable to any virus with a robust in vitro model.
Affiliation: Department of Cell Biology, Harvard Medical School, 240 Longwood Avenue, Boston, MA 02115, USA; Cambridge Institute for Medical Research, University of Cambridge, Hills Road, Cambridge CB2 0XY, UK. Electronic address: firstname.lastname@example.org.Show MeSH
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Mentions: We have previously shown that HCMV UL141 retains the poliovirus receptor (PVR) in the endoplasmic reticulum, inhibiting cell-surface expression and preventing interaction with activating NK receptor DNAM-1. Intracellular PVR accumulates during HCMV infection. In contrast, a second DNAM-1 ligand poliovirus receptor-related 2 (PVRL2) is targeted for proteasomal degradation by UL141 acting with other HCMV gene(s) (Prod’homme et al., 2010; Tomasec et al., 2005). QTV confirmed these results; we observed rapid depletion of PVR from the plasma membrane, in contrast to its accumulation within WCL. PVRL2 was lost from both PM and WCLs (Figure 7). The WCL kinetics of UL141 expression paralleled that of PVR but were inversely related to PVRL2.
Affiliation: Department of Cell Biology, Harvard Medical School, 240 Longwood Avenue, Boston, MA 02115, USA; Cambridge Institute for Medical Research, University of Cambridge, Hills Road, Cambridge CB2 0XY, UK. Electronic address: email@example.com.