Ian Davis

Professional Training and experience

• Bachelor of Anatomical Science (with honours), University of Bristol, Bristol, England
• Bachelor of Veterinary Science (with honours), University of Bristol, Bristol, England
• Clinical Veterinarian, Animal Resources Program, University of Alabama at Birmingham, Birmingham, Alabama
• Predoctoral Fellow, Department of Comparative Medicine, University of Alabama at Birmingham, Birmingham, Alabama
• Ph.D., Pathology, University of Alabama at Birmingham, Birmingham, Alabama
• Research Instructor, Department of Comparative Medicine, University of Alabama at Birmingham, Birmingham, Alabama
• Research Instructor, Department of Anesthesiology, University of Alabama at Birmingham, Birmingham, Alabama
• Research Assistant Professor, Department of Anesthesiology, University of Alabama at Birmingham, Birmingham, Alabama
• Veterinary Medical Officer, Birmingham Veterans' Administration Medical Center, Birmingham, Alabama
• Visiting Assistant Professor, Department of Veterinary Biosciences, The Ohio State University, Columbus, Ohio

Research Interests

Since 2001, my primary research focus has been on the pathophysiologic effects of pulmonary viral infections (hantaviruses, respiratory syncytial virus, and influenza A viruses). I pioneered investigation of the impact of these pathogens on respiratory epithelial ion transport, alveolar fluid clearance, lung mechanics, and nucleotide signaling in vivo, and remain one of the very few investigators in this important field. Over the past 14 years as an independent investigator, I have extended my studies to focus on development of new therapeutics for viral lung injury, the pathogenesis of viral exacerbations of asthma and cystic fibrosis (CF), and the effects of viral infections on lung mechanics and pulmonary responses to b-adrenergic agonists and glucocorticoids. Current research in my laboratory aims to determine the impact of influenza A virus infection on alveolar type II (ATII) epithelial cell function at the single cell level in a mouse model of influenza-induced ARDS. We are primarily focused on investigating the effects of influenza infection on the ATII cell metabolome, with a particular focus on mitochondrial function and cellular energetics. The goal of these studies, which utilize both mouse models and precision cut human and macaque lung slices, is to identify novel host determinants of influenza pathogenesis which can be targeted therapeutically. As part of this work, we have been developing liponucleotides as novel therapeutics for ARDS. Recently we have also begun studies to define the effect of SARS CoV-2 infection on ATII cell function and metabolism. Data from these experiments formed the basis for a clinical trial of the liponucleotide CDP-choline (citicoline) in hospitalized critically ill patients with COVID-19, which recently began enrolling patients.