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Oncolytic herpes simplex virus 1 (oHSV-1) is a genetically engineered double-stranded DNA virus designed to selectively infect, replicate within, and destroy tumor cells. It initiates tumor cell lysis via direct cytopathic effects, including apoptosis, autophagy, necroptosis, and disruption of cellular integrity. Infected cells release tumor antigens and damage-associated molecular patterns (DAMPs), which stimulate both innate and adaptive immune responses, effectively turning the tumor into an "in situ vaccine." Variants such as T-VEC (expressing GM-CSF) and experimental constructs producing cytokines or checkpoint inhibitors have demonstrated efficacy in clinical trials. Despite promising antitumor effects, safety issues related to viral replication, host tissue tropism, and the risk of herpes-related complications remain important therapeutic challenges[1][2][5][3][4].
Selective infection and replication in tumor cells, leading to cell lysis\nInduction of cellular apoptosis, autophagy, and necroptosis\nStimulation of immunogenic cell death, release of tumor antigens and DAMPs\nRecruitment and activation of immune cells (dendritic cells, T cells, NK cells), promoting systemic antitumor immunity and abscopal effect
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