Kurtis M. Host

TL;DR: The findings confirmed the current view that reactive oxygen species can promote mucoidy in vitro, but revealed PMNs are proficient at inducing mucoid conversion in the absence of an oxidative burst, which led to the discovery that cationic antimicrobial peptides can be mutagenic and promoteMucoidy.

TL;DR: A role for MAVS and RIG-I signaling during different stages of the KSHV life cycle is suggested, and it is shown that Rig-I and its adaptor protein, MAVS, can sense K SHV infection and that these proteins can suppress KshV replication following primary infection and/or viral reactivation.

TL;DR: KSHV-mediated PD-L1 increase may represent a novel mechanism of KSHV’smediated immune modulation to allow for virus survival and eventually malignant progression.

TL;DR: It is proposed that the tumor virus Kaposi’s Sarcoma-associated herpesvirus (KSHV) establishes a niche favorable for viral spread and cell transformation through cell-derived vesicles, all while avoiding detection.

TL;DR: This study reports that KSHV stimulates the RIG-I signaling pathway in a RNA polymerase (Pol) III-independent manner and subsequently induces type I interferon (IFN) responses and expands the role of Rig-I by providing an example of a DNA virus activating a canonical RNA-sensing pathway.