Table 2.
Comparison of oncolytic reovirus and bluetongue virus.
| Reovirus* | Bluetongue virus# |
|---|---|
| About 100× more efficient replication in RAS-transformed cancer cells | 5,000× more efficient replication in RAS-transformed cancer cells |
| Produce potent and specific CPEs | Similar results |
| About 3× more efficient proteolytic disassembly (uncoating) because more active endosomal and lysozsomal proteases (cathepsins B and L) are present in cancer cells | Determination in progress |
| Produce 4× more infectious progeny than non-infectious defective interfering particles | Determination in progress |
| About 9× more caspase-induced apoptosis | Has caspase-3 induced apoptosis |
| Caspase-independent apoptosis (NA) | Presence of Caspase-independent apoptosis |
| Poly (I:C) did not prevent reovirus infection | Similar results |
| Pro-inflammatory cytokines (NA) | Higher levels of pro-inflammatory cytokine production |
| Reovirus persistently infected Raji cell, did not reduce xenograft tumor in mice and “cure” cells (Raji) | Data Not Available (NA) |
| HTR1 cell is a highly reovirus-resistant Fibrosacoma cell derived from HT1080. It has reduced cathepsin B activity and it constrains reovirus oncolysis | No BTV-resistant human cancer cells have not been detected yet |
| Persist in tumor through days (NA) | Persist in human tumor xenografts in mice through day 30 from a single injection |
| Toxicity tests are well tolerated | Similar preliminary results |
| Systemic delivery (some success) | Work in Progress |
| Required specific genetic modifications | No modification is required |
| Humans have pre-existing anti-reovirus sera | Humans have no pre-existing anti-BTV sera |
| No integration of viral genome into host cell genome | No integration of viral genome into host cell genome |
| Have done Phase I–II clinical trials and Phase III is ongoing | Work under planning and in progress |