Table 1.
A comparison of three oncolytic viruses: strength and pitfalls
| Virus | VV | Herpes simplex virus (HSV) | Coxsackievirus A21, B3 (CVA21 and CVB3) |
|---|---|---|---|
| Genome | dsDNA (~ 180-Kb, 200 genes) | dsDNA (~ 152-kb, 80 genes) | (+) ssRNA (~ 7.4-Kb, one polyprotein) |
| Capacity of inserted DNA | 25–40 Kb | 30–40 Kb | 300 bases for stable recombinant |
| Tumor selectivity (once inside the cells) | Pexa-Vec: selectively replicates in and destroys cancer cells driven by genetic pathways commonly activated in cancers. | T-VEC: two mutations make up cancer selectivity with activated Ras and high endogenous ribonucleotide reductase | Aberrant signaling pathways within tumor cells On cell surface: CVA21: ICAM-1 dependent. CVB3: CAR dependent |
| Life cycle | Cytoplasm (no risk of integration) | Nucleus (more risk of integration) | Cytoplasm |
| Mechanisms of cell death | Apoptosis and necroptosis (ICD)a | Apoptosis, necrosis, and pyroptosis (ICD) | Immunogenic apoptosis, autophagy (ICD) |
| Immunogenicity | High | High | High |
| Transgene expression | High | High | High |
| Clinical trial stage | Phase III for liver cancer | T-VEC approved for melanoma | Phase II study in advanced melanoma (CVA21) |
aICD immunogenic cell death