Type I interferons such as interferon-β (IFN-β) are indispensable cytokines that defend mammals against viral infections. As a result, subversion of type I interferons is a key evolutionary tactic for viruses in the virus-host arms race. Our lab studies Kaposi’s sarcoma-associated herpesvirus (KSHV), which uses host caspases to prevent IFN-β induction during lytic infection. Inhibiting caspases restores IFN-β induction during KSHV lytic infection. However, the IFN-β produced under these conditions only comes from 3% of infected cells. This heterogeneity of IFN-β induction during viral infection also occurs in infection with other viruses such as flu and SARS-Cov-2. I aim to identify the factors that regulate the heterogeneity of IFN-β induction during KSHV lytic infection.