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Immune-mediated effector molecules can limit cancer growth, but lack of sustained immune activation in the tumour microenvironment restricts antitumour immunity. New therapeutic approaches that induce a strong and prolonged immune activation would represent a major immunotherapeutic advance. Here we show that the arenaviruses lymphocytic choriomeningitis virus (LCMV) and the clinically used Junin virus vaccine (Candid#1) preferentially replicate in tumour cells in a variety of murine and human cancer models. Viral replication leads to prolonged local immune activation, rapid regression of localized and metastatic cancers, and long-term disease control. Mechanistically, LCMV induces antitumour immunity, which depends on the recruitment of interferon-producing Ly6C+ monocytes and additionally enhances tumour-specific CD8+ T cells. In comparison with other clinically evaluated oncolytic viruses and to PD-1 blockade, LCMV treatment shows promising antitumoural benefits. In conclusion, therapeutically administered arenavirus replicates in cancer cells and induces tumour regression by enhancing local immune responses.

Original publication

DOI

10.1038/ncomms14447

Type

Journal article

Journal

Nat Commun

Publication Date

01/03/2017

Volume

8

Keywords

Animals, Arenavirus, CD8-Positive T-Lymphocytes, Cell Line, Tumor, Humans, Immunologic Surveillance, Interferon Type I, Lymphocyte Activation, Lymphocytic choriomeningitis virus, Mice, Inbred C57BL, Monocytes, Neoplasms, Oncolytic Viruses, Programmed Cell Death 1 Receptor, Virus Replication