>90%, by SDS-PAGE under reducing conditions and visualized by silver stain.
<0.10 EU per 1 μg of the protein by the LAL method.
Measured by its ability to inhibit Type-I IFN-mediated anti-viral activity. Symons, J.A. et al. (1995) Cell 81:551. The ED50 for this effect, as measured by inhibition of Recombinant Human IFN‑ alpha 2 (Catalog # 11105-1)
, is typically 0.3-1.8 ng/mL.
The viral type I IFN receptor, B19R, inhibits the anti-viral activity of Recombinant Human IFN‑ alpha 2. The ED50 for this effect is typically 0.3-1.8 ng/mL.
B19R is a 60-65 kDa protein encoded by the Vaccinia virus genome and by the genomes of other orthopoxviruses. Its function represents one of several mechanisms used by these viruses to evade the host immune response (1, 2). It is known as B19R in the Copenhagen strain of Vaccinia and as B18R in the Western Reserve (WR) strain (3). There is a structurally-unrelated, larger Vaccinia protein that is also known as B18R that contains multiple ankyrin-like repeats (4). B19R, however, contains three immunoglobulin-like domains and shows homology to human, mouse, and bovine type I interferon receptors (5). The Wyeth strain of Vaccinia virus encodes a truncated protein that lacks the C-terminal Ig-like domain, and the Lister strain of Vaccinia produces an inactive B19R (6, 7). B19R functions as a decoy binding protein for type I interferons (IFN alpha, beta, omega). It binds to type I interferons from multiple species and prevents IFN signaling through its receptors (6-8). B19R binds to the surface of virus infected and uninfected cells where it retains its capacity to bind and neutralize IFN (6, 8). It shields those cells from the antiviral effects of type I interferons, thereby enabling virus replication and pathogenicity (6-8). B19R also limits the effectiveness of IFN alpha produced following TLR activation (9), and it limits adaptive T cell responses (3).
Smith, G.L. et al. (2013) J. Gen. Virol. 94:2367.
Perdiguero, B. and M. Esteban (2009) J. Interferon Cytokine Res. 29:581.
Gomez, C.E. et al. (2012) J. Virol. 86:5026.
Goebel, S.J. et al. (1990) Virology 179:247.
Smith, G.L. and Y.S. Chan (1991) J. Gen. Virol. 72:511.
Alcami, A. et al. (2000) J. Virol. 74:11230.
Symons, J.A. et al. (1995) Cell 81:551.
Colamonici, O.R. et al. (1995) J. Biol. Chem. 270:15974.
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