Viral replication and destruction of tumor cells alter TME, trigger chemotaxis and accumulation of cytotoxic lymphocytes to the site of infection, and can convert immune “cold” to “hot” tumors; viral replication induces ICD, and releases DAMPs, such as calreticulin, high-mobility group protein B1 (HMGB1) and ATP, along with tumor-associated antigens. Here, HMGB1 is linked to infection.