Ad
| | | | |
hTERT-Ad
|
E1a gene driven by hTERT promoter
|
Immunogenic apoptosis
|
hTERT-Ad and bortezmib (proteasome inhibition) leads to potent antitumor immunity
|
[65]
|
Ad5/3-D24-GMCSF
|
Ad3 fiber E1a-deleted (RB-selective) GM-CSF +
|
Enhanced autophagy; ecto- CRT; released ATP and HMGB1
|
Tumor-specific T cell responses and antitumor efficacy in some patients [clinical trial]
|
[62]
|
HSV
| | | | |
G207
|
R34.5-; ICP6-
|
NA
|
Systemic antitumor immunity (CD8+ T cells)
|
[66]
|
HSV-1716
|
ICP 34.5 gene mutant
|
Induction of IFN-γ, CXCL9 and CXCL10
|
Intratumoral injection increased NK and CD8+ T cells
|
[67]
|
T-VEC
|
ICP47-γ34.5 - GM-CSF +
|
Necrosis/apoptosis (in vivo)
|
Antigen-specific T cell responses and decreases in Treg, Ts, and MDSC in human melanoma patients [clinical trials]
|
[68, 69]
|
HSV-2 ΔPK mutant
|
ICP10 PK domain deleted
|
Apoptosis/Pyroptosis
|
Dominant induction of CD4+ Th1 cells
|
[70]
|
Poxvirus
| | | | |
vSP
|
Spi-1/spi-2-
|
Necrosis/apoptosis HMGB1 release
|
NA
|
[58]
|
vvDD
|
tk-/vgf-
|
Necrosis/HMGB1 and ATP release
|
CD11b + cells and CD11b+Ly6G+ cells (DCs and Neutrophils)
|
[71]
|
Pexa-Vec
|
tk-GM-CSF+
|
NA
|
Antiviral CTL and antibodies against TAAs in Human HCC patients [clinical trial]
|
[72]
|
Arbovirus
| | | | |
VSV-GFP (Indiana serotype)
|
Marker gene GFP
|
Induction of IL-28 by virally activated innate immune cells in the TME
|
IL-28 sensitize cancer cells to NK cell recognition and killing
|
[73]
|
VSVgm-icv oncolytic vaccine plateform
|
Deletion in The M protein at position 51; VSV-GM-CSF+
|
NA
|
The antitumor immunity is robust enough to control established tumor. Tumor is infiltrated by a large number of IFNγ-producing T and NK cells
|
[74]
|
Paramyxovirus
| | | | |
MV-eGFP (Edmonston strain)
|
Marker gene EGFP
|
Released inflammatory cytokines and chemokines; IL-6 and HMGB1
|
Enhance innate antitumor and melanoma-specific adaptive immunity (in vitro)
|
[55]
|
MV vaccine-infected tumor cells
|
Marker gene EGFP
|
ICD; apoptotic cells phagocytosed by DCs
|
Allowing DC to mature, produce high level of IFN-α, and cross-present TAAs and production of tumor-specific CD8 T cells
|
[75, 76]
|