Abstract
Glioma tumors are one of the most devastating cancer types. Glioblastoma is the most advanced stage with the worst prognosis. Current therapies are still unable to provide an effective cure. Recent advances in oncolytic immunotherapy have generated great expectations in the cancer therapy field. The use of oncolytic viruses (OVs) in cancer treatment is one such immune-related therapeutic alternative. OVs have a double oncolytic action by both directly destroying the cancer cells and stimulating a tumor specific immune response to return the ability of tumors to escape the control of the immune system. OVs are one promising alternative to conventional therapies in glioma tumor treatment. Several clinical trials have proven the feasibility of using some viruses to specifically infect tumors, eluding undesired toxic effects in the patient. Here, we revisited the literature to describe the main OVs proposed up to the present moment as therapeutic alternatives in order to destroy glioma cells in vitro and trigger tumor destruction in vivo. Oncolytic viruses were divided with respect to the genome in DNA and RNA viruses. Here, we highlight the results obtained in various clinical trials, which are exploring the use of these agents as an alternative where other approaches provide limited hope.
Highlights
Diffuse gliomas are the most frequent central nervous system (CNS) tumors with an infiltrative growth pattern which includes astrocytoma, oligodendrogliomas, and oligoastrocytomas [1]
The first generation of conditionally replicative adenoviruses (CRad) started with Onyx-015, a chimeric adenovirus generated from two and five serotypes that has a deletion in the E1B-55kD gene and was approved in China for the treatment of head and neck cancer in 2005 [47]
Poliovirus can cause neurotoxicity, Gromeier and colleagues eliminated this by replacing the internal ribosome entry site (IRES) of the poliovirus vaccine Sabin strain with the non-virulent human rhinovirus type 2 (HRV2) [141]
Summary
Diffuse gliomas are the most frequent central nervous system (CNS) tumors with an infiltrative growth pattern which includes astrocytoma, oligodendrogliomas, and oligoastrocytomas [1]. HSV-1 C134 was developed as a chimeric virus that includes the deletion of γ134.5 loci and the expression of human cytomegalovirus (HCMV) IRS1 gene This insertion increases viral replication and lytic effect when administered intrathecally in a murine GBM tumor model inducing antitumor T cell mediated immune responses, which elicit long systemic immune-memory enhancing survival [32,33]. Decrease of tumor regrowth after oncolytic treatment is the objective followed by rapid antiangiogenesis mediated by oncolytic virus (RAMBO) This virus includes deletion of γ134.5 loci, GFP linked to ICP6 carboxyl terminus, and expression of human Vstat120 gene under immediate early IE4/5 HSV promoter. For these reasons, modified HSVs have been assessed for glioma treatment in clinical studies
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