Biography
Douglas J. Perkins, PhD, received a B.S. in Neuroscience, Physiological and Experimental Psychology from The Ohio State University in 1990. He earned an M.S. in Neuropathology in 1992 and a Ph.D. in Molecular Cell Biology and Neuroscience from The Ohio State University in 1997. Following his doctoral training, he completed National Institutes of Health (NIH) T32 postdoctoral fellowships in Hematology, Clinical Immunology, Hematology-Oncology, and Transfusion Medicine at Duke University and served as a Visiting Scientist at the Albert Schweitzer Hospital Tropical Research Unit in Lambaréné, Gabon. He subsequently joined the Centers for Disease Control and Prevention (CDC) as a Scientist in Tropical Medicine before entering academia. Dr. Perkins is currently Distinguished Professor of Medicine, Founding Director of the Center for Global Health, and a Scientist at Los Alamos National Laboratory. His research focuses on malaria pathogenesis, global infectious diseases, host-pathogen interactions, multi-omics, and translational approaches to improving health in resource-limited settings.
Personal Statement
My career has been dedicated to understanding the biological mechanisms that drive severe infectious diseases and translating those discoveries into interventions that improve human health. I have spent more than 25 years conducting translational research on malaria, HIV, COVID-19, and other emerging infectious diseases, with a particular focus on improving outcomes for children and underserved populations in sub-Saharan Africa and the United States.
I am passionate about building sustainable international research partnerships that integrate scientific discovery, clinical care, public health, and workforce development. As the Founding Director of the Center for Global Health at the University of New Mexico, I have established long-term collaborations with academic institutions, hospitals, ministries of health, and research organizations throughout Africa, creating programs that advance research while strengthening local capacity through education and mentorship.
My laboratory employs multidisciplinary approaches, including genomics, transcriptomics, proteomics, immunology, computational biology, and molecular epidemiology, to identify mechanisms of disease pathogenesis and discover novel diagnostic, therapeutic, and precision medicine strategies. More recently, my research has expanded to include vector-borne diseases and statewide surveillance programs that bridge global health and local public health priorities.
Equally important to my research mission is mentoring the next generation of scientists and physician-investigators. Throughout my career, I have had the privilege of training students, postdoctoral fellows, clinicians, and junior faculty from the United States and numerous low- and middle-income countries, many of whom now serve as leaders in academia, government, and global health. I believe that meaningful scientific advances are achieved through collaboration, mentorship, and a commitment to improving health worldwide.
Achievements & Awards
Distinguished Professor of Medicine, University of New Mexico School of Medicine (2025-Present).
Founding Director, Center for Global Health, University of New Mexico (2008-Present).
Community Engagement Award, University of New Mexico 15th Annual Research Excellence (2024).
Top Basic Scientist Award Winner, University of New Mexico 14th Annual Research Excellence (2023).
National Institutes of Health (NIH) T32 Postdoctoral Fellow, Duke University, Divisions of Hematology, Clinical Immunology, Hematology-Oncology, and Transfusion Medicine (1997-1999).
Scientist in Tropical Medicine, Centers for Disease Control and Prevention (CDC), Division of Parasitic Diseases (1999-2001).
Visiting Scientist, Albert Schweitzer Hospital Tropical Research Unit, Lambaréné, Gabon (1998).
Scientist, Los Alamos National Laboratory (2013-Present)
Principal Investigator and Multi-PI on multiple NIH-funded research and training awards, including NIH/NIAID R01, R21, and NIH/Fogarty D43 international research training grants. Total grant funding across 25 years at 53M USD as PI.
Founder and Director of long-standing international research and training partnerships between the University of New Mexico and institutions in Kenya that have trained numerous graduate students, postdoctoral fellows, and physician-scientists from Africa and the United States (>100 trainees).
Research and Scholarship
Molecular Mechanisms of Cytokines, Chemokines, and Effector Molecules. Our group was the first to identify that prostaglandins are suppressed in children with severe malaria, demonstrating that down-regulation of these effector molecules contributes to enhanced pathogenesis of severe disease and mortality. We were also the first to show that chemokines are dysregulated in severe childhood malaria, linking altered immune signaling to suppression of erythropoiesis and increased morbidity and mortality.
Building on these discoveries, we were the first to define molecular mechanisms underlying multiple pathogenic features of severe malaria, including impaired inhibitory leukocyte signaling through reduced LAIR1 expression (Achieng et al., EBioMedicine. 2019;45:278-289), dysregulated T-cell effector responses with altered IFN-? and IL-17 expression (Raballah et al., PLoS One. 2017;12(4):e0175864), and host genetic determinants of susceptibility involving complement component 5 variants (Raballah et al., Front Genet. 2022;13:977810).
More recent work from our group was the first to integrate transcriptomic and proteomic approaches to define dysregulation of HSP60/70-TLR2/4 signaling and altered glutamine metabolism in pediatric severe malarial anemia, establishing mechanistic links between immune signaling, metabolism, and disease severity (Onyango et al., Pathogens. 2024;13(10):867). These studies reflect long-standing collaboration with Dr. Kristan A. Schneider (contact PD/PI), who contributed to the genetic and analytical components of our studies (Raballah et al., Front Genet. 2022;13:977810, Onyango et al., Pathogens. 2024;13(10):867), highlighting the ongoing collaboration underlying the multi-PI structure of this application. These findings collectively establish a unifying framework for immune dysregulation driving severe malaria pathogenesis and identify potential targets for therapeutic intervention.
Host Genetic Factors and Susceptibility to Severe Malaria. Our group was the first to identify host genetic variants that influence susceptibility to severe malaria and related outcomes in African children. Over the past 25 years, we have defined novel genetic determinants regulating susceptibility to pediatric malaria, severe malarial anemia, and all-cause mortality in high-burden settings, providing critical insight into mechanisms driving disease heterogeneity and clinical outcomes. These studies were conducted in Siaya County, Kenya, a holoendemic Plasmodium falciparum transmission setting with intense and repeated exposure, ideal for defining host genetic effects on disease risk. These discoveries include variants in CSF2 associated with longitudinal disease risk (Kisia et al., Trop Med Health. 2022;50(1):41), complement component 5 influencing susceptibility to Plasmodium falciparum infections and severe malarial anemia (Raballah et al., Front Genet. 2022;13:977810), and IFNA2/IFNA8 haplotypes associated with reduced IFN-? and enhanced risk of severe malarial anemia and mortality (Kempaiah et al., Hum Genet. 2012;131:1375-1391).
We were also the first to demonstrate that mutations in complement component 3 alter longitudinal risk of pediatric malaria and severe malarial anemia, establishing a central role for complement pathways in disease pathogenesis and identifying targets for therapeutic intervention (Raballah et al., Exp Biol Med. 2021).
This work is being extended to define genetically regulated immune pathways that can be targeted with existing and novel therapeutics to improve clinical outcomes in high-risk pediatric populations. These studies reflect long-standing collaboration with Dr. Kristan A. Schneider (contact PD/PI), who contributed to the genetic and analytical components of these investigations, supporting the multi-PI structure of this application.