Tumor cell lysis via oncolytic virus infection (null)

Tumor cell lysis via oncolytic virus infection is a therapeutic mechanism where viruses are engineered or selected for their ability to preferentially infect and replicate within cancer cells, ultimately causing the cells to burst (lyse), releasing viral progeny and tumor antigens that stimulate further immune attack on remaining cancer cells[1][2][3][4][5]. Oncolytic viruses take advantage of defects in cancer cell antiviral defenses and, upon replication, not only destroy the tumor directly but also trigger local and systemic antitumor immune responses. These processes include the activation of dendritic cells, T cells, and natural killer cells, and can be further enhanced by engineering the viruses to deliver genes coding for immune stimulatory molecules or cytotoxic proteins[1][2][3][4][5]. Several viruses, such as talimogene laherparepvec, have entered clinical use or late-stage trials, often in combination with immune checkpoint inhibitors or other therapies. Major challenges include immune clearance before the virus acts, delivery barriers in some tumors, and patient selection for optimal efficacy[1]. Importantly, "tumor cell lysis via oncolytic virus infection" is not a discrete molecular target but a therapeutic strategy built on multiple molecular and cellular mechanisms[1][2][3][4][5].

Other names

Oncolytic viral therapyoncolytic virotherapyoncolytic virus-mediated tumor cell deathOV therapy

Selective infection/replication in tumor cells via cell-surface receptor recognition or exploitation of tumor cell antiviral pathway defects; Direct oncolysis (viral replication within tumor cells causes cell lysis and spread of progeny viruses); Induction of immunogenic cell death (release of antigens and danger signals activating dendritic cells, T cells, NK cells); Delivery of transgenes/therapeutic genes into tumor cells (e.g., suicide genes, immunostimulatory cytokines)