- Role: Research ScientistGroup: Regulation of Interferon and Innate Signalling
Dr Natália Sampaio is a postdoctoral researcher working on RNA sensing in the innate immune system. She applies cutting-edge methods to understand how cytosolic RNA receptors, such as MDA5 and PKR, are activated and regulated. She is particularly interested in their role in both viral infection and inflammatory diseases. Dr Sampaio is also investigating how these RNA receptors may respond to novel mRNA therapies, such as the COVID-19 mRNA vaccines.
Dr Sampaio obtained her PhD at the Walter and Eliza Hall Institute in 2016, where she studied innate immune responses and host-pathogen interactions of the malaria parasite Plasmodium falciparum. Following this, she joined the group of Professor Jan Rehwinkel at the University of Oxford, where she investigated cytosolic nucleic acid receptors in the context of viral infection and interferonopathies. In 2021, she returned to Melbourne to join the research group of Professor Paul Hertzog at Hudson Institute, where she established novel lines of investigation on RNA sensing. In 2021, Dr Sampaio was selected as Hudson Institute Emerging Leader. Her work has been supported by both government grants and industry collaborations.
Sampaio NG, et. al. (2021) The RNA sensor MDA5 detects SARS-CoV-2 infection. Sci. Rep. (11) 13638
Dias Junior AG, Sampaio NG, Rehwinkel J. (2018) A balancing act: MDA5 in antiviral immunity and autoinflammation. Trends in Microbiology; DOI 10.1016/j.tim.2018.08.007
Sampaio NG, et al. (2018) Extracellular vesicles from early-stage P. falciparum-infected red blood cells contain PfEMP1 and induce transcriptional changes in human monocytes. Cell. Microbiol., 20(5) e12822
Sisquella X, Ofir-Birinr Y, Pimentel MA, Cheng L, Karam PA, Sampaio NG, et. al. (2017) Malaria parasite DNA-harbouring vesicles activate cytosolic immune sensors. Nat. Commun. 8(1)
Sampaio NG, Eriksson EM, Schofield L. (2017) Plasmodium falciparum protein PfEMP1 modulates monocyte/macrophage transcription factor activation and cytokine and chemokine responses. Infect. Immun.