Table 3.
Tumor Type | OVs | Effects |
---|---|---|
Colorectal cancer | Poxvirus vvDD-CCL11 | increase of immunogenic programmed necrosis antitumor acquired immune response -enhanced levels of IFNγ [110] |
Vaccinia virus GLV-1h68 | Infiltration of NK cells and macrophages-increase of proinflammatory cytokines and chemokines (IFN, IL3, IL6, CXCL10, GCP-2, KC/GRO, lymphotactin, M-CSF1, MIP-1, RANTES, MCP-1, MCP-3 and MCP-5) expression of metallelastase by inflammatory macrophages [111] | |
Glioblastoma | oHSV | oHSV antitumor efficacy is inhibited by: inflammatory macrophage activation in glioma [112,113]-CCN1 activation [114,115] |
oHSV antitumor efficacy is prompted by: M2 macrophage activation with TGF-β [116] | ||
Virus DNX-2401 | increase of the CSF concentration of cytokines (IFNγ, TNF, IL6) and increase of CD64 (M1 polarization marker) [117] | |
H-1PV | infiltration of CTLs, induction of cathepsin B and iNOS expression in TAMs [118] | |
Virotherapy + ICB (anti-CTLA-4, anti- PD-1 and oHSV G47Δ-mIL-12) | influx of macrophages and M1-like polarization in glioma [119] | |
Pancreatic ductal adenocarcinoma | H-1PV | coapplication with IFNγ extended animal survival and IFNγ may enhance MHCII molecule expression on the surface of macrophages and DCs [120] |
OAd-TNFα-IL-2 in combinationwith meso-CAR T cell | increase of CAR T cell and host T cell infiltration to the tumor-polarization toward the M1 phenotype -increase of DC maturation [121] | |
Pancreatic cancer | Immunotherapy + virotherapy Adenovirus TMZ-CD40L | increase of tumor-infiltrating T-cells-switch from M2 to M1 macrophages [122] |
Breast cancer | Paramyxoviruses (measles/mumps) | increase of the antitumor efficacy by macrophages independently of initial polarization status and viral replication [123] |
Oncolytic adenovirus expressing soluble TGFβ receptor II-Fc fused | inhibition of TGFβ in bone metastasis reducing M2-osteoclast activity and tumor progression [124] |
The table reports the effects of oncolytic viruses (OVs) on specific tumor types.