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: email@example.com.Show MeSH
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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).
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.