Maritza Jaramillo

Biography

Dr. Maritza Jaramillo received her undergraduate degree in Biology from Universidad Nacional de Colombia (Bogotá, Colombia). Subsequently, she completed her MSc and PhD in Microbiology and Immunology at Université Laval (Quebec, QC, Canada) under the supervision of Dr. Martin Olivier. During his graduate studies, Dr. Jaramillo worked on the transcriptional regulation of pro-inflammatory molecules induced during protozoan parasitic infections. Subsequently, she began her postdoctoral research in Dr. Nahum Sonenberg’s laboratory at McGill University (Montreal, QC, Canada), where she worked on translational control of infectious diseases. In May 2012 Dr. Jaramillo joined the Faculty of INRS – Centre Armand-Frappier Santé Biotechnologie (CAFSB)  as an Assistant Professor to investigate the mechanisms and the functional consequences of dysregulated mRNA metabolism during toxoplasmosis. In May 2018 Dr. Jaramillo was granted tenure and was promoted to the rank of Associate Professor.

Research Program

Role of dysregulated mRNA turnover and protein synthesis in the pathogenesis of congenital toxoplasmosis

Congenital toxoplasmosis is an infectious disease caused by Toxoplasma gondii (T. gondii), an obligate intracellular parasite commonly transmitted to humans by ingestion of contaminated raw meat, water, or soil. During pregnancy, T. gondii infection can lead to miscarriage, premature births, or serious birth defects (e.g. blindness, hydrocephalus, and mental retardation). It is estimated that ~30-40% of the world population is seropositive and that >90% of women in childbearing age are at risk of contractingthe parasite. Unfortunately, efficient and safe vaccines are lacking and available treatments often display teratogenic side effects. Hence, it has become critical to understand the molecular mechanisms underlying the interactions between T. gondii and the infected patient, particularly at the mother/fetus interface. In light of this problem, Dr. Jaramillo’s group investigates how dysregulation of host mRNA turnover and protein synthesis during T. gondii infection contributes to disrupt normal functions of placental cell populations including resident macrophages and trophoblasts, which are essential for embryo implantation and fetal development. Her studies also rely on the use of clinical samples from infected pregnant women and the ex vivo model of placental explants obtained from healthy donors. These valuable resources help validate data obtained in vitro and assess the implications of such findings in a clinical setting. Dr. Jaramillo’s long-term goal is to advance our understanding of the biological underpinnings implicated during congenital toxoplasmosis and to devise ways to thwart T. gondii transmission to promote healthy pregnancies.

Post-transcriptional regulation of host gene expression during Leishmania infection

Protozoan parasites of the genus Leishmania are the causative agents of leishmaniasis, a group of diseases with clinical symptoms ranging from skin lesions to visceral pathologies that can lead to death if left untreated. Unfortunately no effective vaccine has been developed yet and drug resistance is rapidly increasing. Therefore, the current situation reflects an urgent need to better understand the molecular basis of interactions between Leishmania and its host cell. In infectious diseases, the regulation of mRNA translation allows cells to quickly adjust their proteomes but can also be exploited by the invading pathogen. Leishmania lives inside immune cells called macrophages, one of the most powerful lines of defense against microbial invasion. To survive in this environment, the parasite modulates numerous intracellular signals necessary for the activation of the transcription of genes linked to the immune response. As a result, many functions of the macrophage are affected. Using a genome-wide approach (polysome profiling coupled to RNA-seq), Dr. Jaramillo’s team recently demonstrated that in addition to modifying transcription, Leishmania selectively deregulates mRNA translation in macrophages (Chaparro, Leroux et al. 2020 PLoS Pathogens https://doi.org/10.1371/journal.ppat.1008291). Bioinformatics analyses of identified transcripts suggest that key metabolic, immune and microbicidal functions are hijacked by Leishmania via the modulation of host mRNA translation. Based on these results current projects in Dr. Jaramillo’s laboratory aim to further investigate the mechanisms and functional consequences of the alteration of host mRNA translation in the progression of the disease. To this end, her team utilizes in vitro and in vivo infection models, clinical Leishmania isolates, patient samples from endemic regions, mutant cell lines and transgenic mice in combination with Omics approaches (RNA -seq, CLIP-seq, BRIC-seq, proteomics). These studies will help identify new regulatory nodes of gene expression in macrophages that might contribute to design effective and safe treatments to reduce morbidity and mortality associated with leishmaniasis.

Research Funding

Currently, Dr. Jaramillo’s research program is funded by a CIHR Project Grant (OCT/2019 – SEP/2025) and an NSERC Discovery Grant (APR/2019 – MAR/2025).