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Chris Moore, PhD Adjunct

Chris Moore, PhD

Chris Moore, PhD, is director of immunology at Arbutus Biopharma. Dr. Moore received his master’s and PhD in physiology from North Carolina State University, Raleigh, NC. Dr. Moore then completed a postdoctoral fellowship at the Lineberger Comprehensive Cancer Center at UNC-Chapel Hill. Dr. Moore held the position of adjunct associate professor at Meredith College, Raleigh, NC, and visiting lecturer at North Carolina State University, Raleigh, NC. Dr. Moore was chief scientist and group leader at Glaxosmithkline (GSK) with research focused on host immune responses to infectious diseases. Following GSK, Dr. Moore joined Arbutus Biopharma as director of immunology with research focused exclusively on hepatitis B virus cure.

Following the sequencing of the human genome in 2001, a flurry of research in molecular biology uncovered many previously unknown genes with sequence homology to known immune genes. Chris Moore, PhD’s research was focused on characterizing NLRX1, a unique member of a family of genes named the nod-like receptors (NLRs). Nod proteins are intracellular sentinels for infection with Nod1/Nod2 functioning to mediate intracellular detection of pathogen associated molecular patterns (PAMPs) thereby conferring specificity to host cell innate immune responses. In fact, we now know that much like the toll-like receptors (TLRs), each NLR confers specificity to a unique PAMP and regulates intracellular signaling cascades for pro-inflammatory, antiviral, and cell death responses.

NLRX1 is a Nod-like receptor found to function as a negative regulator of host antiviral responses (Moore, Nature, 2008). Mitochondrial antiviral signaling adaptor (MAVS) protein resides within the mitochondria and mediates RIG-I like receptor (RLR) signaling cascades. Without MAVS, very little type 1 interferon can be produced in response to infection with many classes of viruses. However, this IFN-I response has to be highly regulated as constant activation can lead to host cell death.  NLRX1 was identified as a mitochondrial negative regulator of MAVS signaling through its interaction with the leucine rich repeat (LRR) region. Additionally, mice lacking NLRX1 indeed can eliminate viral infection quicker than wildtype animals through rapid upregulation of IFN-I responses but dysregulation of NFkB and IRF3 leads to concomitant systemic upregulation of pro-inflammatory cytokines leading to immunological shock (Moore, Immunity, 2011). Understanding how each NLR regulates these pathways could lead to the identification of drug targets capable of fine tuning host immunity to infectious disease. In fact, infectious disease drug discovery over the last decade has included a close examination of targets important for both the pathogen life cycle and restoration of natural immune function.

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