Global Health Travel Award Winners Convene at Cell Death Meeting in Brazil

Last week in São Paulo, Brazil, researchers convened for the “Why So Many Ways to Die? Apoptosis, Necroptosis, Pyroptosis, and Beyond” meeting to discuss the latest research in cell death pathways, including roles in cancer, host defense and inflammatory diseases. Among them were approximately three-dozen Global Health Travel Award (GHTA) winners—scientists from low- and middle-income countries selected to attend and present their work alongside field leaders.

Global Health Travel Awards provide scientists from diverse backgrounds and limited resource settings with opportunities afforded by attending top tier scientific conferences, including:

• • Joining conversations at the forefront of research and medicine
  • Sharing their work with global research leaders
  • Gaining access to invaluable networking and career development opportunities
  • Receiving Pre-meeting Workshop Training on the state and direction of the field

Find out more about Global Health Travel Awards

These Awards are made possible in part through funding from The Bill & Melinda Gates Foundation and The Sao Paulo Research Foundation (FAPESP), a public foundation supported by local tax payers with the mission to support research projects in higher education and research institutions, and other Foundation support.

See upcoming Global Health Travel Award Opportunities and Deadlines

One of these Global Health Travel Award winners is hometown native Dr. Renan V.H. de Carvalho, a post-doctoral researcher at the University of São Paulo, who also celebrated the publication of his work in Nature Communications during the meeting!

Here Dr. de Carvalho shares what it’s like to be a Global Health Travel Awardee, and provides insights from his recent publication on Leishmania.

Interview with Dr. Renan V.H. de Carvalho

How did the GHTA Pre-Meeting Workshop prepare you for the meeting?

RC: The Pre-meeting Workshop was coordinated by Karina Bortoluci, Petr Broz, Andreas Strasser and Domagoj Vucic, giving the Awardees an overview about the main types of cell death and their implications in health and disease.

It was a fantastic experience, particularly for those who were not so familiar with these themes. The detailed explanation of the different types of cell death provided an early immersion in these themes and the workshop was extremely important; to understand the latest discoveries discussed during the Meeting.

What did you learn in the Pre-Meeting Workshop that will help you to advance your research and/or career?

RC: The issues pointed out during the Pre-Meeting Workshop outlined which types, and aspects, of cell death, are still only beginning to be investigated, demonstrating that there is still so much to learn and discover in the near future.

What does your new publication tell us about how the Leishmania parasite manipulates the host’s “so many ways to die” to its own benefit?

RC: Activation of the inflammasome by parasites can lead to a form of cell death called pyroptosis-- the main described inflammasome, NLRP3, is an important innate pathway involved in Leishmaniasis.

In our recent study combining human and mouse experimental models, we show that:

• Some species of Leishmania parasites harbor an endosymbiotic virus (LRV)
• LRV manipulates host immune responses, blocking NLRP3 activation and favoring parasite replication.        

This work helps to explain a long-standing question in the field; how LRV and other factors contribute to mucocutaneous Leishmaniasis, a disfiguring form of the disease.

How does Leishmania do this alone, and how does its viral partner help?

RC: Although Leishmania alone does not induce cell death, it does induce NLRP3 inflammasome activation and IL-1b derived from this platform helps to control infection. The virus (LRV) limits this activation of the inflammasome, favoring parasite replication and disease exacerbation.

Are there other examples of such microbial cooperation in parasitic or bacterial infections?

RC: Yes, there are other viruses described to infect other protozoan or multicellular parasites. However, the relevance of such endosymbiosis for infection in other organisms is not fully understood. Our work unravels that question and demonstrates how LRV favors mucocutaneous disease in the context of Leishmaniasis.

How does the host immune system try to leverage different “ways to die” to fight Leishmania infection?

RC: This is a question that is still open in the field of Leishmania. Interestingly, cell death is barely induced in vitro upon infection. We speculate that the parasite has evolved to avoid cell death since host cells are their replicative niche.

What do your discoveries tell us about better treating Leishmania infection?

RC: With the findings described in our article, we now suggest that every patient diagnosed with Leishmaniasis, should also be screened for the presence of the virus.

We hope that, in the near future, patients that are LRV+ should have a differential clinical treatment, with specific blockers or activators of the pathways that we recently identified in our study.

What was most valuable for you in attending this meeting?

Thanks to the Global Health Travel Award I got the opportunity to see outstanding new science and unpublished studies and met different scientists working on cell death and related topics. This was extremely valuable for me.

I also got to know lots of new colleagues, expanding my network in the world of science. I enjoyed many fruitful discussions with top scientists in the field, who provided great research suggestions and shifted my mindset to be even more of a forward-thinking researcher.

Read Dr. de Carvalho's Publication:

Leishmania RNA virus exacerbates Leishmaniasis by subverting innate immunity via TLR3-mediated NLRP3 inflammasome inhibition

For more insights into the “Why So Many Ways to Die?” meeting, see our social media, blog and video coverage below:

@KestoneSymp #KScelldeath