Enhancing the HSV-1-mediated antitumor immune response by suppressing Bach1.

ABSTRACT:

Background

In 2015, herpes simplex virus 1 (HSV-1)-derived talimogene laherparepvec (T-VEC) was the first oncolytic virus approved by the US Food and Drug Administration as a therapeutic agent for cancer treatment. However, its antitumor application is limited to local treatment of melanoma, and there is a lack of understanding of the mechanisms underlying the regulation of HSV-1 replication in cancer cells and the associated antitumor immunity. We hypothesized that increasing the replication capacity of HSV-1 in tumor cells would enhance the antitumor effect of this virus.

Methods

We systematically identified IFN-stimulated genes induced by HSV-1 by performing functional screens and clarified the mechanism by which BACH1 acts against HSV-1. Then, we tested the effect of BAC

SUBMITTER: Pan C 

PROVIDER: S-EPMC8976103 | biostudies-literature | 2022 Apr

REPOSITORIES: biostudies-literature