Disease relevance of PVR

• The expression of PVR and/or Nectin-2 was less frequent in lymphoblastic leukemias [1].
• Thus, assessment of the PVR surface levels may represent a novel useful criterion to predict the susceptibility/resistance of neuroblastomas to NK-mediated killing [2].
• Analysis of the ligands for triggering NK receptors revealed the consistent expression of Poliovirus receptor (PVR) and Nectin-2 in myeloid leukemias [1].
• The human receptor for poliovirus (CD155) is an immunoglobulin-like molecule with unknown normal function(s) [3].
• Its function in adults is as yet unknown, but significantly, CD155 is aberrantly expressed in neuroectodermal tumors [4].

Psychiatry related information on PVR

• Incompetent patient (PVS): decision-making, courts and the family -- In re Tavel [5].
• While there is growing support for withdrawing/withholding food and water (assisted nutrition and hydration, or "AHN") from people described as being in a "persistent vegetative state" ("PVS") and people with other profound neurological impairments, such as advanced dementia, the issue remains controversial, and for many, unresolved [6].

High impact information on PVR

• Northern hybridization analysis indicates that poliovirus receptor transcripts are expressed in a wide range of human tissues, in contrast to the limited expression of virus binding sites, which suggests that additional factors or modifications of the receptor protein are required to permit poliovirus attachment [7].
• The predicted amino acid sequence reveals that the human poliovirus receptor is an integral membrane protein with the conserved amino acids and domain structure characteristic of members of the immunoglobulin superfamily [7].
• This membrane glycoprotein is poliovirus receptor-related protein 1 (Prr1), designated here as HveC [8].
• Altogether, our results demonstrate that DNAM-1 regulates monocyte extravasation via its interaction with PVR expressed at endothelial junctions on normal cells [9].
• In the present paper, we show that PVR and Nectin-2 are expressed at cell junctions on primary vascular endothelial cells [9].

Chemical compound and disease context of PVR

• The fit was confirmed by the location of carbohydrate moieties in the CD155 glycoprotein, the conserved properties of elbow angles in the structures of cell surface molecules with Ig-like folds, and the concordance with prior results of CD155 and poliovirus mutagenesis [10].
• In the patients with pulmonary hypertension, PVR fell significantly after inhaled NO and after prostacyclin [11].
• Treatment of SOFIA cells with 5-azacytidine restored susceptibility to poliovirus infection, which correlated with the appearance of PVRs at the cell surface, as detected with anti-PVR monoclonal antibody D171 [12].
• Eleven patients, with advanced chronic obstructive lung disease (COLD), received an infusion of the calcium antagonist felodipine at a rate of 0.9 mg/h. Pulmonary and systemic vascular resistances (PVR and SVR) at rest were reduced by 18% (p less than 0.05) and 33% (p less than 0.001), respectively [13].
• METHODS: Forty-one men over the age of 50 years with an American Urological Association (AUA) symptom score greater than 8, postvoid residual urine volume (PVR) less than 300 mL, and no clinical or biochemical evidence of prostate cancer were treated with terazosin independent of the baseline PFR [14].

Biological context of PVR

• CD155 (poliovirus receptor) localizes in cell-matrix adhesions and cell-cell junctions, but its role in the regulation of cell adhesion and cell motility has not been investigated [15].
• We confirmed the interaction biochemically and by co-immunoprecipitation, and we mapped the Tctex-1 binding site to a SKCSR motif within the juxtamembrane region of CD155 [16].
• In addition, overexpression of Gli1 or Gli3 potently activates reporter gene expression driven by the CD155 core promoter [4].
• The predicted amino acid sequences indicate that PVR alpha and PVR delta, corresponding to the previously described cDNA clones H20A and H20B, respectively, are integral membrane proteins while the other two molecules described here for the first time lack a putative transmembrane domain [17].
• In situ hybridization using a cDNA fragment as a probe demonstrated that the PVR gene is located at the band q13.1----13.2 of human chromosome 19 [17].

Anatomical context of PVR

• DNAM-1 and PVR regulate monocyte migration through endothelial junctions [9].
• Because DNAM-1 is highly expressed on leukocytes, we investigated the role of the DNAM-1-PVR interaction during the monocyte transendothelial migration process [9].
• In vitro, both anti-DNAM-1 and anti-PVR mAbs strongly blocked the transmigration of monocytes through the endothelium [9].
• Indeed, PVR-expressing neuroblastomas were efficiently killed by NK cells [2].
• We propose that the cytoplasmic domain may target CD155-containing endocytic vesicles to the microtubular network [16].

Associations of PVR with chemical compounds

• The human poliovirus receptor/CD155 is a transmembrane glycoprotein belonging to the immunoglobulin superfamily [4].
• We also demonstrated in glutathione S-transferase pull-down experiments that the dynein light chain, Tctex-1, interacts directly with the cytoplasmic domain of hPVR [18].
• One of the cell lines expressed a mutant of hPVR, in which both asparagine residues of the two N-glycosylation sites of the V domain were changed to aspartate (N105D) and serine (N120S), respectively [19].
• Necl-5 regulates cell movement and proliferation cooperatively with integrin alphavbeta3 and growth factor receptors [20].
• A Harken prosthetic disc valve (DVR) was used in 53 patients and glutaraldehyde-preserved Hancock porcine xenograft (PVR) in 56 patients [21].

Physical interactions of PVR

• Here we provide evidence that CD155 binds specifically to vitronectin with a dissociation constant (K(d)) of 72 nM as determined by surface plasmon resonance [3].
• Necl-5 does not directly bind afadin and therefore is not associated with cadherins [22].
• Herpes simplex virus glycoprotein D can bind to poliovirus receptor-related protein 1 or herpesvirus entry mediator, two structurally unrelated mediators of virus entry [23].
• DNase I footprinting using recombinant hAP-2alpha indicated that this transcription factor bound to both the FPI and FPII regions of the CD155 core promoter fragment [24].

Regulatory relationships of PVR

• PVR cell surface expression was detected on most mononuclear cells expressing CD14, a marker for mononuclear phagocytes [25].

Other interactions of PVR

• HIgR shares its ectodomain with and appears to be an alternative splice variant of the previously described protein PRR-1 (poliovirus receptor-related protein) [26].
• Comparison of the deduced amino acid sequences of PVR orthologs revealed that the NH(2)-terminal immunoglobulin-like domain (domain 1), which is the virus binding site in the human PVR, is highly variable among species, whereas that of PRR1 is highly conserved [27].
• One of them, named necl-5, which does not homophilically trans-interact, but heterophilically trans-interacts with nectin-3, regulates cell migration and adhesion [28].
• These data support the interpretation that CD155 (and related proteins) are physically associated with CD44 on monocyte cell surfaces [29].
• Overall, our findings do not support a role of HVEB and PVR genes in the development of MS [30].

Analytical, diagnostic and therapeutic context of PVR

• The structure of the extracellular, three-domain poliovirus receptor (CD155) complexed with poliovirus (serotype 1) has been determined to 22-A resolution by means of cryo-electron microscopy and three-dimensional image-reconstruction techniques [10].
• Immunofluorescence analysis of poliovirus receptor expression in Peyer's patches of humans, primates, and CD155 transgenic mice: implications for poliovirus infection [31].
• We first demonstrate the existence of soluble CD155 (sCD155) isoforms in culture medium conditioned by CD155-expressing cells, in human serum and in cerebrospinal fluid. sCD155 concentration was measured in human serum and cerebrospinal fluid using a specific ELISA [32].
• The acute effects of inhaled nitric oxide (NO) (40 ppm in air) on pulmonary (PVR) and systemic (SVR) vascular resistance were compared with those of an intravenous infusion of prostacyclin (24 micrograms/h) in 8 patients with severe pulmonary hypertension and 10 cardiac patients with normal values of PVR [11].
• Cardiac catheterization in the 6 patients with CHF revealed severe PHT, increased pulmonary resistance (PVR), and normal capillary wedge pressure [33].

References