Experience

Unifesp - Universidade Federal de São Paulo

• Brazil
• Higher Education
• 700 & Above Employee

• Associate Professor

  • Oct 2010 - Present

  In a previous work, we showed that vesicles released by infective forms of Trypanosoma cruzi, the agent causative of Chagas' disease, modulate the inflammatory responses and the infection in cultured cells and animals. Our group showed also have shown that virulent strains of T. cruzi release more vesicles in vitro when compared to less virulent isolates of the parasite. The present project aims initially to characterize the composition and quantity of vesicles of different isolates of the parasite and then correlate these with the infectivity in cultured cells and experimental animal models. As the vesicles have an immunomodulatory effect, parallel studies will evaluate the role of these vesicles in a model of infection by Influenza virus. This work will help to demonstrate the role of these vesicles as immunomodulatory factors and verify whether these factors also act in other models of infection.2012-2015 - CNPq - (Processo Universal 470425/2012-1) 2012-2014 - Mecanismos imunomoduladores de vesículas liberadas da membrana do Trypanosoma cruzi. FAPESP (2012/50226-2) 2016 - 2017 2016/12111-0 Cross-Organism Communication by Extracellular Vesicles: Hosts, Microbes, Parasites - FAPESP (2016/12111-0) 2016 – FAPESP 2016/01917-3 O papel imunomodulatório das vesículas extracelulares liberadas por macrófagos infectados pelo Trypanosoma cruzi - US$ 100,000.002018 –"In vivo Proof-of-Concept (PoC) studies in the mouse model of acute Chagas disease" – DNDi



Weizmann Institute of Science

• Israel
• Research
• 700 & Above Employee

• Visiting Professor

  • Nov 2019 - Jan 2020



The University of Georgia

• Higher Education
• 700 & Above Employee

• Postdoctoral Research Associate

  • Feb 2010 - Jan 2011

  During my post-doctoral training (second). I studied a RNA interference (RNAi) methodology and genome-wide assay to identify candidate host genes that are required during influenza replication, our laboratory has identified and validated numerous host cell factors that could be potential drug targets for blocking key events required for influenza virus replication in host cells. To determine if CDC25B is a druggable target for regulating influenza virus replication, we evaluated NSC95397, a specific inhibitor of CDC25B phosphatase on influenza virus replication in BEAS2B cells. The cell culture pre-incubated with NSC 95397 and subsequently infected with A/WSN/33 virus had dramatically reduced levels of virus copies at 24h as determined by qRT-PCR. These results confirm that CDC25B phosphatase has an important role in influenza virus replication. CDC25B and CaMKIIB inhibitors (KN-93) do not affect virus entry but have an additive effect in preventing influenza viral replication. To determine if the compounds act at different steps in the virus life cycle, where treatment would have an additive effect on inhibiting virus replication, we tested their combined effect on virus replication. The results showed that KN-93 when given at suboptimal concentrations has an additive effect in the CDC25B inhibitor. Therefore, both compounds act in different steps of virus replication. These findings also suggest that simultaneously targeting of CAMKIIB and CDC25B might decrease the efficacy against the influenza virus. We tested the effect of this compound in a mouse model of influenza virus infection. The prophylactic treatment with NSC 95397 inhibits Influenza A virus in lung after 24 and 48 hours after infection. The results from our studies show NSC95397 inhibition of CDC25B phosphatase mice effectively blocks influenza virus replication in vitro and in vivo suggesting that targeting CDC25B phosphatase could be a valuable therapeutic approach to treat influenza infection.



Instituto de Química - USP

• Postdoctoral Research Fellow

  • Nov 2004 - Dec 2008

  During my post-doctoral training, I studied the role of these vesicles on the in vivo T. cruzi infection in the murine model. Our data suggest that, similar to what was observed in vitro, the vesicles generate a strong inflammatory response in vivo. We demonstrated that these membranes increase inflammatory reaction and produced more parasites in the tissues and a severe heart pathology. This severe pathology was due to an increase of CD4 and CD8 cells with a decrease of iNOS producing. At the same time high levels of IL-4 and IL-10 were observed