Oncolytic virotherapy has produced promising yet limited results in preclinical and clinical studies. Besides direct oncolytic activity, a significant therapeutic mechanism of oncolytic virotherapy is the induction of tumor-specific immunity. Consequently, the efficacy of oncolytic viruses can be improved by the insertion of immune stimulator genes and rational combinatorial therapy with other immunotherapies. This article reviews recent efforts on arming oncolytic viruses with a variety of immune stimulator molecules, immune cell engagers, and other immune potentiating molecules. We outline what is known about the mechanisms of action and the corresponding results. The review also discusses recent preclinical and clinical studies of combining oncolytic virotherapy with immune-checkpoint inhibitors and the role of oncolytic virotherapy in changing the tumor microenvironment.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8411207 | PMC |
http://dx.doi.org/10.1016/j.omto.2021.05.002 | DOI Listing |
J Med Virol
January 2025
National Key Laboratory of Veterinary Public Health and Safety, College of Veterinary Medicine, China Agricultural University, Beijing, China.
Oncolytic viruses are emerging as promising cancer therapeutic agents, with several poxviruses, including vaccinia virus (VACV) and myxoma virus, showing significant potential in preclinical and clinical trials. Modified vaccinia virus Ankara (MVA), a laboratory-derived VACV strain approved by the FDA for mpox and smallpox vaccination, has been shown to be incapable of replicating in human cells unless zinc finger antiviral protein (ZAP) is repressed. Notably, ZAP deficiency is prevalent in various cancer types.
View Article and Find Full Text PDFMol Cancer Ther
December 2024
Augusta University, Augusta, Georgia, United States.
Glioblastoma (GBM) is the most frequent malignant brain tumor. We recently discovered that oncolytic herpes simplex virus engineered to disable tumor-intrinsic protein kinase R (PKR) signaling (oHSV-shPKR) could increase oHSV oncolysis and anti-tumor immune response. However, here we show that disabling tumor-intrinsic PKR signaling can also induce the activation of the indoleamine 2,3-dioxygenase (IDO) signaling pathway.
View Article and Find Full Text PDFMol Biol (Mosk)
December 2024
Mechnikov Research Institute for Vaccines and Sera, Moscow, 105064 Russia.
The sensitivity of human glioblastoma cells to virus-mediated oncolysis was investigated on five patient-derived cell lines. Primary glioblastoma cells (Gbl13n, Gbl16n, Gbl17n, Gbl25n, and Gbl27n) were infected with tenfold serial dilutions of the Leningrad-3 strain of the mumps virus, and virus reproduction and cytotoxicity were monitored for 96-120 h. Immortalized human non-tumor NKE cells were used as controls to determine the virus specificity.
View Article and Find Full Text PDFNat Commun
December 2024
Department of Biomedicine, Aarhus University, 8000, Aarhus C, Denmark.
J Neurooncol
December 2024
Department of Neurosurgery, McGovern Medical School, The University of Texas Health Science Center, 6400 Fannin Street, Suite # 2800, Houston, TX, 77030, USA.
Purpose: This systematic review aimed to collate and synthesize the available literature on the abscopal effect in Glioblastoma multiforme (GBM) neoplasms, focusing on the reported biochemical mechanisms driving the abscopal effect.
Methods: A systematic search was conducted in PubMed, Cochrane Database of Systematic Reviews, and Epistemonikos from inception to May 1, 2023. Studies exploring the abscopal effect in GBM were included.
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!