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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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Temporal Changes in Known and Putative Cell-Surface Immunomodulators(A) Temporal profiles of known NK ligands whose modulation by HCMV had not previously been recognized.(B) Temporal profiles of T cell ligands not previously known to be modulated during infection.(C) Temporal profiles of all quantified protocadherins.(D) Validation of the temporal profile of PDCHγC3 by flow cytometry.Red diamonds, 12 hr after infection with irradiated HCMV. See also Figure S4, Table S5, and Data S1.
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fig4: Temporal Changes in Known and Putative Cell-Surface Immunomodulators(A) Temporal profiles of known NK ligands whose modulation by HCMV had not previously been recognized.(B) Temporal profiles of T cell ligands not previously known to be modulated during infection.(C) Temporal profiles of all quantified protocadherins.(D) Validation of the temporal profile of PDCHγC3 by flow cytometry.Red diamonds, 12 hr after infection with irradiated HCMV. See also Figure S4, Table S5, and Data S1.

Mentions: We mined our data for all known NK cell ligands (Vivier et al., 2008) and discovered previously unrecognized modulation of six ligands during HCMV infection. E-cadherin (CDH1), the ligand for the inhibitory NK receptor KLRG-1 (killer cell lectin-like receptor subfamily G member 1), was dramatically upregulated during infection. Vascular cell adhesion molecule 1 (VCAM1) and B7-H6, ligands for activating NK receptors α4β1 integrin and NKp30, were downregulated (Figure 4A). Interestingly, other known ligands including collagen I (COL1A1 and COL1A2), collagen III (COL3A1), cell adhesion molecule-1 (CADM1), and poliovirus receptor-related 1 (PVRL1) were expressed in a manner that would be expected for an appropriate response to intracellular infection (Figure 4A; Table S2).


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)

Temporal Changes in Known and Putative Cell-Surface Immunomodulators(A) Temporal profiles of known NK ligands whose modulation by HCMV had not previously been recognized.(B) Temporal profiles of T cell ligands not previously known to be modulated during infection.(C) Temporal profiles of all quantified protocadherins.(D) Validation of the temporal profile of PDCHγC3 by flow cytometry.Red diamonds, 12 hr after infection with irradiated HCMV. See also Figure S4, Table S5, and Data S1.
© Copyright Policy - CC BY
Related In: Results  -  Collection

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

fig4: Temporal Changes in Known and Putative Cell-Surface Immunomodulators(A) Temporal profiles of known NK ligands whose modulation by HCMV had not previously been recognized.(B) Temporal profiles of T cell ligands not previously known to be modulated during infection.(C) Temporal profiles of all quantified protocadherins.(D) Validation of the temporal profile of PDCHγC3 by flow cytometry.Red diamonds, 12 hr after infection with irradiated HCMV. See also Figure S4, Table S5, and Data S1.
Mentions: We mined our data for all known NK cell ligands (Vivier et al., 2008) and discovered previously unrecognized modulation of six ligands during HCMV infection. E-cadherin (CDH1), the ligand for the inhibitory NK receptor KLRG-1 (killer cell lectin-like receptor subfamily G member 1), was dramatically upregulated during infection. Vascular cell adhesion molecule 1 (VCAM1) and B7-H6, ligands for activating NK receptors α4β1 integrin and NKp30, were downregulated (Figure 4A). Interestingly, other known ligands including collagen I (COL1A1 and COL1A2), collagen III (COL3A1), cell adhesion molecule-1 (CADM1), and poliovirus receptor-related 1 (PVRL1) were expressed in a manner that would be expected for an appropriate response to intracellular infection (Figure 4A; Table S2).

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