Overview of the pre-clinical and clinical studies about the use of CAR-T cell therapy of cancer combined with oncolytic viruses

Abstract

Background Cancer is one of the critical issues of the global health system with a high mortality rate even with the available therapies, so using novel therapeutic approaches to reduce the mortality rate and increase the quality of life is sensed more than ever. Main body CAR-T cell therapy and oncolytic viruses are innovative cancer therapeutic approaches with fewer complications than common treatments such as chemotherapy and radiotherapy and significantly improve the quality of life. Oncolytic viruses can selectively proliferate in the cancer cells and destroy them. The specificity of oncolytic viruses potentially maintains the normal cells and tissues intact. T-cells are genetically manipulated and armed against the specific antigens of the tumor cells in CAR-T cell therapy. Eventually, they are returned to the body and act against the tumor cells. Nowadays, virology and oncology researchers intend to improve the efficacy of immunotherapy by utilizing CAR-T cells in combination with oncolytic viruses. Conclusion Using CAR-T cells along with oncolytic viruses can enhance the efficacy of CAR-T cell therapy in destroying the solid tumors, increasing the permeability of the tumor cells for T-cells, reducing the disturbing effects of the immune system, and increasing the success chance in the treatment of this hazardous disease. In recent years, significant progress has been achieved in using oncolytic viruses alone and in combination with other therapeutic approaches such as CAR-T cell therapy in pre-clinical and clinical investigations. This principle necessitates a deeper consideration of these treatment strategies. This review intends to curtly investigate each of these therapeutic methods, lonely and in combination form. We will also point to the pre-clinical and clinical studies about the use of CAR-T cell therapy combined with oncolytic viruses.

Verification of genetic differences and immune cell infiltration subtypes in the neuroblastoma tumour microenvironment during immunotherapy

“…GD2 and B7H3 chimeric antigen receptor (CAR) T cells maintained high metabolic fitness comparable to resting T cells, were highly resistant to exhaustion and have great in vivo efficacy [ 28 ]. Using of the oncolytic viruses along with Ganglioside GD2-specific CAR-T cells to treat the neuroblastoma led to an increase in the attraction and survival of the CAR-T cells [ 29 ]. However, the inconsistency of the results of previous exploratory studies of tumour surface markers highlights the necessity of determining the ideal subgroup of NB patients for immunotherapy, which is still a major challenge in immunotherapy.…”

Efficacy and safety of oncolytic virus combined with chemotherapy or immune checkpoint inhibitors in solid tumor patients: A meta-analysis

“…Carrier cells were targeted at the tumor site and then infected tumor cells by OV replication and lysing, which exerted the maximum effect and effectively avoided anti-viral response. Another study reported that OVs improved the efficacy of CAR-T cell therapy ( Zarezadeh Mehrabadi et al, 2022 ), which suggested a potential method for cancer treatment. Recently, a clinical trial on binary oncolytic adenovirus in combination with HER2-specific autologous CAR VST, advanced HER2 positive solid tumors has been in process (NCT03740256), which might provide more supporting evidence in the OV combination.…”

Application of oncolytic virus in tumor therapy

“…The other is through the activation of antitumor immunity. OVs induce immunogenic cell death of tumor cells to release a variety of molecules, including pathogen‐associated molecular pattern molecules (PAMPs), damage‐associated molecular pattern molecules (DAMPs), tumor‐associated antigens (TAAs), and tumor‐associated neoantigens 43 . Tumor cells and immune cells activate the expression of inflammatory factors through PAMPs/DAMPs mode, such as type I IFN, interleukin (IL)−1β, IL‐6, IL‐12, TNF‐α, granulocyte macrophage colony‐stimulating factor (GM‐CSF) 44–46 .…”