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Gene Review

PVRL2  -  poliovirus receptor-related 2 (herpesvirus...

Homo sapiens

Synonyms: CD112, HVEB, Herpes virus entry mediator B, Herpesvirus entry mediator B, HveB, ...
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Disease relevance of PVRL2


High impact information on PVRL2


Biological context of PVRL2

  • In conclusion, the analysis of a very large data set suggests that genetic polymorphisms in PVRL2 may influence MS severity and supports the possibility that viral factors may contribute to the clinical course of MS, consistent with previous reports [9].
  • Mutations in region II, patterned after a reported single-nucleotide polymorphism in nectin-2, enhanced intracellular accumulation of both nectin-1 and nectin-2 and had a deleterious effect on all of the activities under study [10].
  • In situ hybridization allowed us to map PRR2 to the 19q13.2-q13.4 bands of the human genome, in the same chromosomal region as PVR [11].
  • Amino acid differences at seven positions in the N termini of the glycoproteins D (gDs) specified by herpes simplex virus type 1 (HSV-1) and HSV-2 are largely responsible for the significantly higher cell fusion activity of HSV-2 gD with Chinese hamster ovary cells expressing human nectin-2 or only an endogenous hamster receptor [12].
  • Cells transfected with the dynamin 3 construct had less uniformly distributed nectin 2 at intercellular contacts when compared to control cells expressing only nectin 2 or transfected with the DsRed plasmid alone [13].

Anatomical context of PVRL2

  • Conversely, FACS analysis and immunostaining demonstrated that extravillous trophoblast cells expressed HveA, HveB, and HveC, and these cells were efficiently infected by HSV vectors [14].
  • HveB was expressed in some human neuronal cell lines, fibroblastic cells, keratinocytes, and primary activated T lymphocytes [15].
  • Antibodies specific for HveB blocked infection of HveB-expressing CHO cells and a human fibroblastic cell strain HEL299 [15].
  • CONCLUSION: The relationship between the PRR2 Sau96I (A/G) polymorphism and early onset coronary artery disease may be due to linkage disequilibrium with the APOE gene and underrepresentation, or a protective effect, of the epsilon2 allele [16].
  • Nectin-2(-/-) mice have shown male-specific infertility, disrupted Sertoli-spermatid junctions and morphologically impaired spermatid development [17].

Physical interactions of PVRL2


Other interactions of PVRL2

  • Here, we examined relationships between a PRR2 Sau96I (A/G) polymorphism, the epsilon2, 3 and 4 alleles of APOE and CHD [16].
  • Susceptibility of the virus-producing target cells to NK cell lysis was partially reversed by blocking ULBP-1 or CD112 with specific antibodies [18].
  • Overall, our findings do not support a role of HVEB and PVR genes in the development of MS [19].
  • The structures of these three components are discussed, with particular emphasis on the molecular mechanisms by which E-cadherin and nectin-2 promote cell adhesion [20].

Analytical, diagnostic and therapeutic context of PVRL2


  1. Analysis of the receptor-ligand interactions in the natural killer-mediated lysis of freshly isolated myeloid or lymphoblastic leukemias: evidence for the involvement of the Poliovirus receptor (CD155) and Nectin-2 (CD112). Pende, D., Spaggiari, G.M., Marcenaro, S., Martini, S., Rivera, P., Capobianco, A., Falco, M., Lanino, E., Pierri, I., Zambello, R., Bacigalupo, A., Mingari, M.C., Moretta, A., Moretta, L. Blood (2005) [Pubmed]
  2. Glycoprotein D homologs in herpes simplex virus type 1, pseudorabies virus, and bovine herpes virus type 1 bind directly to human HveC(nectin-1) with different affinities. Connolly, S.A., Whitbeck, J.J., Rux, A.H., Krummenacher, C., van Drunen Littel-van den Hurk, S., Cohen, G.H., Eisenberg, R.J. Virology (2001) [Pubmed]
  3. The poliovirus receptor CD155 mediates cell-to-matrix contacts by specifically binding to vitronectin. Lange, R., Peng, X., Wimmer, E., Lipp, M., Bernhardt, G. Virology (2001) [Pubmed]
  4. Nectin2alpha (PRR2alpha or HveB) and nectin2delta are low-efficiency mediators for entry of herpes simplex virus mutants carrying the Leu25Pro substitution in glycoprotein D. Lopez, M., Cocchi, F., Menotti, L., Avitabile, E., Dubreuil, P., Campadelli-Fiume, G. J. Virol. (2000) [Pubmed]
  5. DNAM-1 and PVR regulate monocyte migration through endothelial junctions. Reymond, N., Imbert, A.M., Devilard, E., Fabre, S., Chabannon, C., Xerri, L., Farnarier, C., Cantoni, C., Bottino, C., Moretta, A., Dubreuil, P., Lopez, M. J. Exp. Med. (2004) [Pubmed]
  6. Mutations in herpes simplex virus glycoprotein D that prevent cell entry via nectins and alter cell tropism. Manoj, S., Jogger, C.R., Myscofski, D., Yoon, M., Spear, P.G. Proc. Natl. Acad. Sci. U.S.A. (2004) [Pubmed]
  7. Multidirectional interactions are bridging human NK cells with plasmacytoid and monocyte-derived dendritic cells during innate immune responses. Chiesa, M.D., Romagnani, C., Thiel, A., Moretta, L., Moretta, A. Blood (2006) [Pubmed]
  8. Restoration of E-cadherin-based cell-cell adhesion by overexpression of nectin in HSC-39 cells, a human signet ring cell gastric cancer cell line. Peng, Y.F., Mandai, K., Nakanishi, H., Ikeda, W., Asada, M., Momose, Y., Shibamoto, S., Yanagihara, K., Shiozaki, H., Monden, M., Takeichi, M., Takai, Y. Oncogene (2002) [Pubmed]
  9. Allelic association of sequence variants in the herpes virus entry mediator-B gene (PVRL2) with the severity of multiple sclerosis. Schmidt, S., Pericak-Vance, M.A., Sawcer, S., Barcellos, L.F., Hart, J., Sims, J., Prokop, A.M., van der Walt, J., DeLoa, C., Lincoln, R.R., Oksenberg, J.R., Compston, A., Hauser, S.L., Haines, J.L., Gregory, S.G. Genes Immun. (2006) [Pubmed]
  10. Mutations in the N-terminal domains of nectin-1 and nectin-2 reveal differences in requirements for entry of various alphaherpesviruses and for nectin-nectin interactions. Struyf, F., Martinez, W.M., Spear, P.G. J. Virol. (2002) [Pubmed]
  11. The human PRR2 gene, related to the human poliovirus receptor gene (PVR), is the true homolog of the murine MPH gene. Eberlé, F., Dubreuil, P., Mattei, M.G., Devilard, E., Lopez, M. Gene (1995) [Pubmed]
  12. Differences in the N termini of herpes simplex virus type 1 and 2 gDs that influence functional interactions with the human entry receptor Nectin-2 and an entry receptor expressed in Chinese hamster ovary cells. Zago, A., Spear, P.G. J. Virol. (2003) [Pubmed]
  13. The role of dynamin 3 in the testis. Vaid, K.S., Guttman, J.A., Babyak, N., Deng, W., McNiven, M.A., Mochizuki, N., Finlay, B.B., Vogl, A.W. J. Cell. Physiol. (2007) [Pubmed]
  14. Syncytiotrophoblast is a barrier to maternal-fetal transmission of herpes simplex virus. Koi, H., Zhang, J., Makrigiannakis, A., Getsios, S., MacCalman, C.D., Strauss, J.F., Parry, S. Biol. Reprod. (2002) [Pubmed]
  15. A cell surface protein with herpesvirus entry activity (HveB) confers susceptibility to infection by mutants of herpes simplex virus type 1, herpes simplex virus type 2, and pseudorabies virus. Warner, M.S., Geraghty, R.J., Martinez, W.M., Montgomery, R.I., Whitbeck, J.C., Xu, R., Eisenberg, R.J., Cohen, G.H., Spear, P.G. Virology (1998) [Pubmed]
  16. The poliovirus receptor related 2 (PRR2) and apolipoprotein E genes and coronary heart disease. Freitas, E.M., Phan, T.C., Herbison, C.E., Christiansen, F.T., Taylor, R.R., Van Bockxmeer, F.M. Journal of cardiovascular risk. (2002) [Pubmed]
  17. Role of cell adhesion molecule nectin-3 in spermatid development. Inagaki, M., Irie, K., Ishizaki, H., Tanaka-Okamoto, M., Miyoshi, J., Takai, Y. Genes Cells (2006) [Pubmed]
  18. The switch from latent to productive infection in epstein-barr virus-infected B cells is associated with sensitization to NK cell killing. Pappworth, I.Y., Wang, E.C., Rowe, M. J. Virol. (2007) [Pubmed]
  19. The role of the polio virus receptor and the herpesvirus entry mediator B genes for the development of MS. Rosche, B., Cepok, S., Stei, S., Vogel, F., Grummel, V., Hoffmann, S., Kroner, A., Mäurer, M., Rieckmann, P., Sommer, N., Hemmer, B. J. Neuroimmunol. (2004) [Pubmed]
  20. Plasma membrane components of adherens junctions (Review). Blaschuk, O.W., Rowlands, T.M. Mol. Membr. Biol. (2002) [Pubmed]
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