During viral infection, the innate immune system utilizes a variety of specific intracellular sensors to detect virus-derived nucleic acids and activate a series of cellular signaling cascades that produce type I IFNs and proinflammatory cytokines and chemokines. Kaposi’s sarcoma-associated herpesvirus (KSHV) is an oncogenic double-stranded DNA virus that has been associated with a variety of human malignancies, including Kaposi’s sarcoma, primary effusion lymphoma, and multicentric Castleman disease. Infection with KSHV activates various DNA sensors, including cGAS, STING, IFI16, and DExD/H-box helicases. Activation of these DNA sensors induces the innate immune response to antagonize the virus. To counteract this, KSHV has developed countless strategies to evade or inhibit DNA sensing and facilitate its own infection. This review summarizes the major DNA-triggered sensing signaling pathways and details the current knowledge of DNA-sensing mechanisms involved in KSHV infection, as well as how KSHV evades antiviral signaling pathways to successfully establish latent infection and undergo lytic reactivation.

The gene encoding an enzyme from a firefly, discovered at the Sorocaba campus of the Federal University of São Carlos (UFSCar) in Brazil, has given rise to a biosensor capable of detecting pH changes in mammalian cells—which could be useful, for example, in studying diseases and assessing the toxicity of a drug candidate.

The luciferase from the species Amydetes vivianii changes color from bluish-green to yellow and red as acidity decreases in fibroblasts, the most common cell type in connective tissue. It does so with great intensity and stability, something that had not been achieved with other luciferases tested by the research group.

The work is published in the journal Biosensors.