• Curator, COVID-19 Research Registry, American Society for Microbiology

My long-term research interest is the identification of key molecular and cellular mechanisms at the pathogen-host interface that could be exploited as potential targets for the treatment of multiple chronic inflammatory as well as acute, fatal diseases. A current focus of my laboratory is the elucidation of innate immunity networks that, during viral infection and non-infectious insult, might contribute to immunopathology, with a focus in the central nervous system (CNS) and hematopoietic cells. In addition, we are starting to investigate the role of innate immune dysregulation in neurodegenerative diseases, including Alzheimer’s disease. A third focus is to elucidate how non-replicative cellular senescence affects innate immunity pathways. My lab uses molecular and cell biology, immunology, genetics, biochemistry, and animal and cell models to investigate these mechanisms.

Graduate students: NIH-funded position available in neuroimmunology

I have a long-term research interest in understanding the role of innate immune response in health and disease with the ultimate goals of generating scientific knowledge and identifying novel therapeutic targets. I have dedicated part of my career to the discovery of novel mechanisms that contribute to detrimental immunopathogenesis during viral infections, including important human pathogens such as hepatitis C virus, human immunodeficiency virus (HIV-1) and coronaviruses.

More recently, my research program is focused on the elucidation of novel innate immune pathways in the central nervous system (CNS) in response to RNA virus infection and sterile insults. My current research involves two major projects. The first focuses on the role of non-coding RNAs, including microRNAs, in the molecular regulation of neuroinflammation, and the identification of glia-specific responses. The second major project is directed toward the discovery of novel mechanisms underlying inflammation-induced CNS dysfunction and neurodegeneration.

As a mentor, my goal is to foster an environment of scientific excellence and personal development that supports lab members in reaching their full potential. We have a supportive, collaborative and open lab. I welcome potential students who are driven by curiosity and passion. Science doesn’t thrive by asking safe questions.

Immunohistochemistry of brain section (C57BL/6J mice) at day 5 post-infection with a neurovirulent coronavirus
 

Multiple mechanisms by which RNA viruses can manipulate the host RNA interference (RNAi) pathway for enhanced replication.Swaminathan G, Martin-Garcia J, Navas-Martin S. Physiol Genomics. 2013 Nov 15;45(22):1035-48. doi: 10.1152
 

Toll-like receptor 3 (TLR3) participates in both defense and offense in host immunity to viruses. Perales-Lionares, R and Navas-Martin, S. Immunology, 2013 Oct;140(2):153-67. doi: 10.1111/imm.12143

Mobilized: Drexel Researchers Face Down The Coronavirus
Pulse Fall 2020

Selected Publications (See all Sonia Navas-Martin's publications in PubMed.)

“Induction of a Senescence-Like Phenotype in Cultured Human Fetal Microglia During HIV-1 Infection”
Chen NC, Partridge AT, Tuzer F, Cohen J, Nacarelli T, Navas-Martín S, Sell C, Torres C, Martín-García J
Journal of Gerontology. A Biol Sci Med Sci. doi: 10.1093/gerona/gly022, Feb 5, 2018

“Hepatitis C virus core protein enhances HIV-1 replication in human macrophages through TLR2, JNK, and MEK1/2-dependent upregulation of TNF-α and IL-6”
Swaminathan G, Pascual D, Rival G, Perales-Linares R, Martín-García J, Navas-Martín S
FEBS Letters; 588(18):3501-10. DOI: 10.1016/j.febslet.2014.08.009. Sep 17, 2014

“Interplay between microRNAs, Toll-like receptors, and HIV-1: potential implications in HIV-1 replication and chronic immune activation”
Swaminathan G, Navas-Martín S, Martín-García J
Discovery Medicine;18(97):15-27, Jul-Aug 2014

“MicroRNAs and HIV-1 infection: antiviral activities and beyond”
Swaminathan G, Navas-Martín S, Martín-García J
Journal of Molecular Biology; 426(6):1178-97. doi: 10.1016/j.jmb.2013.12.017, Mar 20, 2014

“Toll-like receptor 3 in viral pathogenesis: friend or foe?”
Perales-Linares R and Navas-Martin S.
Immunology; 140(2):153-67. doi: 10.1111/imm.12143, Oct 2013

“RNA viruses and microRNAs: challenging discoveries for the 21st century”
Swaminathan G, Martin-Garcia J, Navas-Martin S
Physiological Genomics;45(22):1035-48. doi: 10.1152/physiolgenomics.00112.2013, Nov 15, 2013

"MicroRNAs, Hepatitis C Virus, and HCV/HIV-1 Co-Infection: New Insights in Pathogenesis and Therapy"
Gupta A, Swaminathan G, Martín-García J, and S Navas-Martín
Viruses, 4(11), 2485-2513, 2012

"A role for microRNA-155 modulation in the anti-HIV-1 effects of Toll-like receptor 3 stimulation in macrophages"
Swaminathan G, Rossi F, Sierra LJ, Gupta A, Navas-Martín S, and J Martín-García
PLoS Pathogens, 8: doi:10.1371/journal.ppat.1002937, 2012

"Protective role of Toll like Receptor 3-induced type I interferon in murine coronavirus infection of macrophages"
Mazaleuskaya L, Veltrop R, Ikpeze N, Martin-Garcia J, and S Navas-Martín
Viruses, 4(5): 901-923, 2012

"Hepatitis B and C virus hepatocarcinogenesis: lessons learned and future challenges"
Bouchard MJ, and S Navas-Martin
Cancer Letters, 305(2): 123-143, 2011

"The V1-V3 region of a brain-derived HIV-1 envelope glycoprotein determines macrophage tropism, low CD4 dependence, increased fusogenicity and altered sensitivity to entry inhibitors"
F. Rossi, B. Querido, D. Nimmagadda, S. Cocklin, S. Navas-Martín, and J. Martín-García
Retrovirology, 5:89, 2008

"Replicase genes of murine coronavirus strains A59 and JHM are interchangeable: differences in pathogenesis map to the 3' one-third of the genome"
S. Navas-Martín, M. Brom, M.M. Chua, R. Watson, Z. Qiu, and S.R. Weiss
Journal of Virology, 81(2): 1022-1026, 2007

"Murine coronavirus evolution in vivo: functional compensation of a detrimental amino acid substitution in the receptor binding domain of the spike glycoprotein"
S. Navas-Martín and S. R. Weiss
Journal of Virology, 79: 7629-7640, 2005

"Coronavirus replication and pathogenesis: implications for the recent outbreak of SARS, and the challenge for vaccine development"
S. Navas-Martín and S. R. Weiss
Journal of Neurovirology, 10: 75-85, 2004

"The spike protein of murine coronavirus determines the ability of the virus to replicate in the liver and cause hepatitis"
S. Navas, S.H. Seo, M.M. Chua, J. Das Sarma, S.T. Hingley, E. Lavi, and S.R. Weiss
Journal of Virology, 75:2452-2457, 2001

Dr. Sonia Navas-Martin presented at the American Society for Microbiology (ASM) COVID-19 Registry Virtual Journal Club (VJC) on November 18th, 2021. Based on Dr. Navas-Martin's expertise in Coronavirus pathogenesis and immunology, she presented the latest information on mRNA vaccines-induced T cell responses and SARS-CoV-2 variants of concern leading the discussion with panelists: Dr. Michael Betts, Perelman School of Medicine, University of Pennsylvania; Dr. Alba Griffoni, Center for Infectious Disease and Vaccine Research, La Jolla Institute for Immunology; and Dr. Andres Finzi, CHUM Research Center, University of Montreal. The journal club was moderated by Dr. Rozanne Sandri-Goldin, editor in chief of the Journal of Virology and assistant curator-in-chief of the ASM Registry. Dr. Navas-Martin was appointed curator of the ASM COVID-19 Registry in 2020.