UC San Diego

Intrinsic antiviral immunity is a critical mediator against viral infection. It is composed of both constitutively expressed antiviral restriction factors and others that are upregulated during infection. Research over the past several years has shown that while type-I and -III IFNs have been traditionally thought to be the primary drivers of the intrinsic antiviral immune response, type-II IFN has clear antiviral capabilities as well - although many of the details remain shrouded in mystery. Our lab recently showed that PARP13, a robust restriction factor capable of attenuating a wide variety of viruses, has two isoforms with distinctly different functions in type-I IFN signaling. Here, we show that PARP13L, but not PARP13S, is required for IFN-γ-mediated inhibition of Sindbis Virus, and potentially other alphaviruses as well. We additionally show that PARP13L is not upregulated by IFN-γ and that other members of the PARP family are involved, and lastly describe future directions for the preliminary data shown here.