Skip to main content

Table 2 Vaccinia virus (VV) encodes multiple genes whose products modulate immune responses

From: Vaccinia virus-mediated cancer immunotherapy: cancer vaccines and oncolytics

Viral genes Key function Relevant findings References
A41L chemokine binding protein Deletion of A41L enhances VV immunogenicity and vaccine efficacy [175]
A44L 3beta-HSD enzyme (v3beta-HSD) A44L promotes steroid synthesis [41, 176]
A46R TLR inhibitor and putative IL-1 antagonist A46R is an inhibitor of the TLR4 signaling pathway [41]
A49 Triggers Wnt signaling A49 targets β-TrCP and thus affects multiple cellular pathways, including the NF-κB and Wnt signaling cascades [40]
A52R Putative inhibitor of TLR signaling A52R targets Toll-like receptor signaling complexes to suppress host defense [38]
A53R Soluble TNF receptor The gene deleted virus retains high immunogenicity but replication is attenuated [177]
B5R Inhibits complement Anti-B5 (EV protein) antibody-directed cell lysis via complement is a powerful mechanism for clearance of infected cells [148]
B8R IFN-γ soluble receptor B8R is a type II IFN binding protein [36, 178]
B13R (SPI-2) Inhibits IL-1β converting enzyme B13R is a nonessential immune-modulating gene that has antiapoptotic and anti-inflammatory properties with sequence homology to serine protease inhibitors (serpins) [179]
B15R IL-1β soluble receptor Deletion led to increased dendritic cell, natural killer cell, and neutrophil migration, as well as chemokine/cytokine expression [36, 38]
B18R IFN-α/β soluble receptor B18R encodes a secreted decoy receptor with a broad antagonizing effect against type I IFNs. It is good for viral replication [180]
C3L (VCP) Complement control protein (VCP) VCP modulates adaptive immune responses during infection [181, 182]
C6 Binds to STA2 and inhibits type I IFN signaling C6 is a dual function protein that inhibits the cellular responses to type I IFNs and as an inhibitor of IRF-3 activation [183]
C7L Antagonizes IRF1-induced antiviral activities C7L inhibits antiviral activities induced by Type I interferons [184, 185]
C12L Binds and inhibits IL-18 C12L promotes virulence by reducing gamma interferon production and natural killer and T-cell activity [41, 186]
E3L Binds dsRNA to block PKR activation E3 protein prevents the antiviral action of ISG15 [187]
F1L Inhibits cytochrome C F1L promotes virulence by inhibiting inflammasome activation [188]
K1L Inhibits NF-κB activation K1L supports viral replication in human cells. Deletion of the gene led to a virus that is less pathogenic due to muted innate immune responses, yet still elicits protective immunity [39]
K3L The dsRNA-activated protein kinase (PKR) is inhibited by this pseudosubstrate inhibitor K3L prevents phosphorylation of e1F2α [189, 190]
K7R Promotes histone methylation associated with heterochromatin association K7R is a virulence gene; it inhibits the NF-κB pathway and thus the migration of neutrophil cells. It affects the acute immune response [37, 38, 191, 192]
M1L Associates with apoptosome The current model is that M1L associates with and allows the formation of the apoptosome, but prevents apoptotic functions of the apoptosome [193]
N1L Inhibits NF-κB N1L is a Bcl-2-like anti-apoptotic protein. It inhibits the NK cell response [194]
  1. Due to the limitation of the number of references that can be cited for this journal, not all relevant papers can be listed