Hi Tina
Dr Worth and Jeff have already provided comprehensive answers, so just sharing some info specific on T-VEC, which reinforces their answers above.
About T-VEC:
Talimogene laherparepvec (T-VEC) is the first oncolytic virus therapy approved by the United States Food and Drug Administration (in 2015) for the treatment of advanced-stage melanoma. As you pointed out, it is a modified oncolytic herpes virus. Despite a paucity of Phase III trials for T-VEC as a therapy for non-melanoma cancers such as SCC, successful off-label use of T-VEC for this purpose has been reported in the literature [1] Case reports, case series, and Phase I and Phase II trials have shown that T-VEC has demonstrated efficacy for non-melanoma cancers [1]
Mode of action
T-VEC is injected locally into the tumor and then selectively recognizes, infects, and destroys malignant cells with minimal effects on normal human cells.[2]
Oncolytic viruses selectively target cancer cells, and their replication within these cells induces tumor cell lysis. As with other injectable agents, local oncolysis is thought to activate T cells that may induce a distant immune response [2]. Several preclinical studies support this by demonstrating tumor infiltration by CD8+ T cells in noninjected metastases [2]
Use with HBOT (experimental study)
An experimental study evaluated the effect of HBOT combined with oncolytic herpes simplex virus on the growth of solid tumor (U87 human glioblastoma cell line) implanted subcutaneously in mice [4]
42 days after tumor implantation authors found that tumors treated with:
- control (saline) showed 80-fold growth of the tumor
- oncolytic herpes simplex virus alone showed a 7-fold growth of the tumor
- hyperbaric oxygen+oncolytic herpes simplex virus exhibited 22-fold growth of the tumor
- erythropoietin+oncolytic herpes simplex virus exhibited 25-fold growth of the tumor
Even though tumors treated with HBOT+oncolytic herpes simplex virus didn't suppress tumor growth as much as oncolytic virus alone, tumor growth in that group was still significantly smaller than in the control group. In this experimental study though, mice didn't have any condition that warranted the use of HBOT, such as soft tissue radiation or bone necrosis (i.e, an approved indication). As with any experimental study, evidence is considered of lower certainty compared with evidence derived from a randomized controlled clinical trial. Assuming similar results were observed clinically, if there was another condition for which HBOT would be warranted (e.g. soft tissue radiation, osteoradionecrosis), HBOT benefits would most likely justify the decrease (if any) in the effects of oncolytic herpes simplex virus on the tumor, as this therapy would still be much more effective in killing tumor cells compared with placebo or no therapy, and patient would benefit from HBOT treatment for the condition being treated.
[1]
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8675341/[2]
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4519012/[3]
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8336507/[4]
https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC2823294/