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Quantitative temporal viromics: an approach to investigate host-pathogen interaction.

Weekes MP, Tomasec P, Huttlin EL, Fielding CA, Nusinow D, Stanton RJ, Wang EC, Aicheler R, Murrell I, Wilkinson GW, Lehner PJ, Gygi SP - Cell (2014)

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.

View Article: PubMed Central - PubMed

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: mpw1001@cam.ac.uk.

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QTV Provides Mechanistic Insights into Downregulated Cell-Surface Targets(A) Proteins that are known to be sequestered within the cell accumulated in WCL samples during infection.(B) Proteins targeted for lysosomal or proteasomal degradation declined during infection.Red diamonds, 12 hr after infection with irradiated HCMV. See also Figures S7A and S7B.
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fig7: QTV Provides Mechanistic Insights into Downregulated Cell-Surface Targets(A) Proteins that are known to be sequestered within the cell accumulated in WCL samples during infection.(B) Proteins targeted for lysosomal or proteasomal degradation declined during infection.Red diamonds, 12 hr after infection with irradiated HCMV. See also Figures S7A and S7B.

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.


Quantitative temporal viromics: an approach to investigate host-pathogen interaction.

Weekes MP, Tomasec P, Huttlin EL, Fielding CA, Nusinow D, Stanton RJ, Wang EC, Aicheler R, Murrell I, Wilkinson GW, Lehner PJ, Gygi SP - Cell (2014)

QTV Provides Mechanistic Insights into Downregulated Cell-Surface Targets(A) Proteins that are known to be sequestered within the cell accumulated in WCL samples during infection.(B) Proteins targeted for lysosomal or proteasomal degradation declined during infection.Red diamonds, 12 hr after infection with irradiated HCMV. See also Figures S7A and S7B.
© Copyright Policy - CC BY
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4048463&req=5

fig7: QTV Provides Mechanistic Insights into Downregulated Cell-Surface Targets(A) Proteins that are known to be sequestered within the cell accumulated in WCL samples during infection.(B) Proteins targeted for lysosomal or proteasomal degradation declined during infection.Red diamonds, 12 hr after infection with irradiated HCMV. See also Figures S7A and S7B.
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.

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.

View Article: PubMed Central - PubMed

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: mpw1001@cam.ac.uk.

Show MeSH
Related in: MedlinePlus