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. Author manuscript; available in PMC: 2010 Apr 1.
Published in final edited form as: Biomaterials. 2009 Jan 29;30(11):1989–2005. doi: 10.1016/j.biomaterials.2008.11.025

Table 3.

Possible viral or bacterial agents for biomimetic immune evasive design

Bioactive Element Sources Effects Ref
Viral Agents
Cytokine response modifier A protein (CrmA) Cowpox virus (CPV) Inhibits the production of caspase-1.
Prevents formation of mature IL-1β from pro-IL-1β.		 [22, 24]
vIL-10 Epstein Barr virus (EBV)
Human cytomegalovirus (HCMV)
Orf virus (OV)		 Produces homologue to pro-wound healing and anti-inflammatory IL-10. [22, 26, 28]
vVEGF OV Binds to VEGFR2. Induces pro-wound healing and pro-inflammatory effects of VEGF. [22, 29]
vTNFR CPV
HCMV		 Secreted to bind to TNF class of cytokines.
Inhibits effect of TNF.		 [22, 131]
vIL-18BP EBV
OV
Molluscum contagiosum virus (MCV)		 Binds to IL-18. Inhibits IL-18-dependent IFN-γ production. [22, 132]
vGM-CSFBP EBV Binds to granulocyte macrophage colony stimulating factor. Modulates colony formation of macrophages. [22, 133]
vMIP2 Kaposi’s sarcoma- associated virus (KSHV) Binds MIP2. Inhibits chemokine effect for immune evasion. [22, 134]
vCKBP2 Vaccinia virus Interacts with receptor binding domain of monocyte chemoattractant protein-1 (MCP-1). Blocks chemokine-receptor interactions. [22, 135]
MT-7 Human myxoma virus (HMV) Binds to chemokine binding motifs on GAGs in extracellular matrix. Disables the chemokine from binding. No chemokine gradient may be formed and maintained. [16, 22, 108, 136]
Bacterial Agents
Cytokine-specific proteases Porphyromonas gingivalis Arg-specific HRGP and RGP2 and Lys- specific KGP proteases degrade TNF-α, eliminating one of major mediators of inflammation. [59]
Protein A Staphylococcus aureus Protein A binds to the Fc region of IgG antibodies. Once bound, the IgG molecules are in the incorrect conformation for recognition from neutrophils or macrophages [116]
Extracellular fibrinogen-binding protein (Efb) Staphylococcus aureus Efb, is a virulence factor that is able to bind to complement components, C3b. Is able to inhibit complementary opsonization. [117, 118]
Clumping factor A (ClfA) Staphylococcus aureus ClfA is the main fibrinogen-binding protein found in S. aureus during the stationary phase of growth. Through surface deposition of fibrinogen, the material becomes anti-opsonic. [119]