Herpes simplex virus type 1 (HSV-1)

Herpes simplex virus type 1 (HSV-1) is a large, enveloped double-stranded DNA virus best known as the causative agent of herpes simplex infections. In the context of cancer therapy, HSV-1 is genetically engineered to preferentially infect and lyse cancer cells—a process termed oncolysis. These oncolytic HSV-1 vectors, such as talimogene laherparepvec (T-VEC), are further modified to enhance tumor selectivity and stimulate antitumor immunity, often by inserting immunostimulatory genes like GM-CSF. Upon infection, the virus replicates in tumor cells, leading to cell lysis, release of tumor antigens, and subsequent activation of the host's immune response against the malignancy. HSV-1-based oncolytic virotherapy is currently clinically approved for certain advanced melanoma cases, with safety mitigated by deletion of neurovirulence and immune evasion genes; use in other cancers is under active investigation. Safety concerns include the risk of viral reactivation, infection in immunosuppressed individuals, and off-target effects, though these risks are minimized with engineered viral vectors and antiviral drugs[1][2][3].

Other names

Herpes simplex virus 1HSV-1Oncolytic HSV-1

Selective infection and lysis of tumor cells (oncolysis); Stimulation of antitumor immunity (especially with GM-CSF-armed viruses)[1][2]; Expression of immunogenic transgenes to enhance local immune responses (e.g., GM-CSF in T-VEC)[1][2]