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Oncolytic virotherapy, a revolutionary tool for cancer treatment has shown promising results for the last two decades. In cancer treatment the patient's safety is of utmost importance and treatment, using oncolytic viruses seems to be the most promising in this aspect. Currently, several viruses including vaccinia virus, coxsackievirus, adenovirus, reovirus, herpes simplex virus, and measles virus are being extensively investigated and are undergoing clinical trials for use in the treatment of various types of advanced cancers. Considering their therapeutic efficacy, safety, and reduced side effects, the use of such engineered viruses in biological cancer therapy has the potential to establish a milestone in cancer research.
A general mechanistic understanding of OV action is emerging in which therapeutic efficacy is achieved by a combination of selective tumor cell killing and establishment of antitumor immunity. It is thought that most oncolytic viruses function through a combination of tumor cell lysis and stimulation of innate and adaptive immunity through presentation of viral and tumor antigens.
Fig. 1 Generalized overview of mechanisms of action of oncolytic viruses.
A diverse range of viruses has been investigated as potential cancer therapeutics. The individual characteristics of OVs currently in clinical trials are summarized below.
HSV has been considered and developed as an oncolytic virus for cancer therapy since 1991. There are seven HSV-based oncolytic viruses among which T-VEC (Commercial name Imlygic) has been approved by US-FDA and European Medicine Agency for clinical use after the successful phase I, II, and III clinical trials. This oncolytic virus was generated by deleting the ICP34.5 and ICP47 genes, and inserting two copies of human granulocyte-macrophage colony-stimulating factor (GM-CSF) gene in place of ICP34.5.
In normal cells, viral replication is blocked by protein kinase R (PKR) activation and subsequent phosphorylation of eukaryotic initiation factor 2 (eIF2). In cancer cells, the disrupted PKR-eIF2 pathway causes uncontrolled cell proliferation and unlimited permissiveness to viral replication as well. ICP34.5 causes dephosphorylation of eIF2 and blocks PKR-induced disruption of protein synthesis. Deletion of ICP34.5 in T-VEC ensures abortive infection in normal cells thereby enabling its replication to be cancer cell-specific. ICP47 decreases the immune destruction caused by the host cell thereby supporting HSV1 proliferation. Deleting ICP47 therefore allows immune destruction of the virus in normal cells while enhancing the cell surface expression of MHC1 in cancer cells and increasing the tumor antigen presentation by the infected cancer cells. The GM-CSF engineered into T-VEC enhances T-cell priming by dendritic cells, thereby stimulating the immune system.
Most of the adenovirus-based oncolytic viruses showed success in clinical trials. Onyx-015 is an adenovirus-based oncolytic virus. Clinical trials involving Onyx-015 were done for the patients with HNSCC, pancreatic cancer, ovarian cancer, colorectal cancer, and premalignant oral dysplasia.
DNX-2401 is another promising adenovirus-based oncolytic virus. It consists of a deletion of 24 bps in the E1A region and the engineering of the RGD motif into the HI-loop of the fiber knob. While this insertion of the RGD-4C motif enhances the replication and infectivity of the adenovirus in cancer cells, it reduces the sequestration of adenovirus by CAR-expressing normal cellsCitation37 thus emphasizing the potency and safety of DNX-2401.
ICOVIR-7 and ICOVIR-5 are two types of oncolytic adenoviruses generated by the Targovax and Catalonia Institute of Oncology, respectively. ICOVIR −7 has been evaluated in a clinical trial for 21 patients with advanced and refractory solid tumors. Anti-tumor activity was observed in this clinical trial, showing stabilization or reduction in tumor size. The results were 1PR, 2MR, and 2SD, indicating its eligibility for further clinical trials. A dose-escalation phase I clinical trial on metastatic melanoma patients showed that the virus could be used for successful systemic administration. However, it failed to induce tumor regression.
Measles virus (MV) belongs to the paramyxoviridae family which also consists of mumps and other viruses that cause respiratory tract infections. The extremely safe live-attenuated MV vaccine was derived following multiple passages in human kidney cells, human amnion cells, and chicken embryos following its isolation from the Edmonstonstrain. With respect to safety, the MV vaccine is very promising as the risk of reverting back of the non-segmented genome into the pathological form is very unlikely. This feature of the MV vaccine is therefore very reliable when it comes to the matter of oncolytic viruses where safety is of utmost importance.
Presently, many oncolytic viruses are undergoing clinical trials for applications in single therapy or combination therapy, and most of them are safe and show almost no dose-limiting toxicities. Therefore, the use of oncolytic viruses in cancer biotherapy has the potential to be an ideal and painless therapeutic option for the cancer patients in future if the above-mentioned challenges are appropriately dealt with.
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