Summary
The co-evolution between hosts and their parasites is one of the most fascinating examples of evolutionary adaptation. However, there is a paucity of information on how the human immune system co-adapts to the parasites phenotypic plasticity, and how it dynamically rearranges its molecular phenotypes aiming to counteract the pathogenic threats. Hence, many therapies for the treatment of intracellular bacteria-related infection (e.g., tuberculosis) are currently obsolete, especially because of the rise in drug resistance. In this framework, the main goal of my proposal is to decipher the unexplored phenotype ‘bar-codes’ of host-pathogen interaction, in order to reversely engineer a drug delivery platform aiming to target infected cells only, and to eradicate intracellular parasites. The final aim will be that of eradicating the severe intracellular pathogens Mycobacterium tuberculosis (Mtb), as it is the major cause of mortality related to bacterial infection worldwide. According to the World Health Organisation, in fact, approximately one-third of the world’s population is asymptomatically affected by TB, with about 9 million new cases of per year (of which 11% are children under 15 years), and 1.4 million of deaths. Despite decades of control programs, TB is still second only to HIV as the greatest killer worldwide due to a single infectious agent (the average killing rate of TB is 3 people per minute). This project will thus explore the molecular bases of Mtb-host interaction. These investigations will be used to engineer 'super-selective' polymeric nanoparticles targeting infected cells only (thus avoiding side effects), and to eradicate intracellular parasite. This will be done while adopting strategies that counteract the development drug resistance. Hence, this project will avoid falling in what has been called as the potential new ‘Dark Middle Age” era of lack of antibiotics.
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| Web resources: | https://cordis.europa.eu/project/id/795224 |
| Start date: | 01-10-2018 |
| End date: | 30-09-2020 |
| Total budget - Public funding: | 170 121,60 Euro - 170 121,00 Euro |
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Original description
The co-evolution between hosts and their parasites is one of the most fascinating examples of evolutionary adaptation. However, there is a paucity of information on how the human immune system co-adapts to the parasites phenotypic plasticity, and how it dynamically rearranges its molecular phenotypes aiming to counteract the pathogenic threats. Hence, many therapies for the treatment of intracellular bacteria-related infection (e.g., tuberculosis) are currently obsolete, especially because of the rise in drug resistance. In this framework, the main goal of my proposal is to decipher the unexplored phenotype ‘bar-codes’ of host-pathogen interaction, in order to reversely engineer a drug delivery platform aiming to target infected cells only, and to eradicate intracellular parasites. The final aim will be that of eradicating the severe intracellular pathogens Mycobacterium tuberculosis (Mtb), as it is the major cause of mortality related to bacterial infection worldwide. According to the World Health Organisation, in fact, approximately one-third of the world’s population is asymptomatically affected by TB, with about 9 million new cases of per year (of which 11% are children under 15 years), and 1.4 million of deaths. Despite decades of control programs, TB is still second only to HIV as the greatest killer worldwide due to a single infectious agent (the average killing rate of TB is 3 people per minute). This project will thus explore the molecular bases of Mtb-host interaction. These investigations will be used to engineer 'super-selective' polymeric nanoparticles targeting infected cells only (thus avoiding side effects), and to eradicate intracellular parasite. This will be done while adopting strategies that counteract the development drug resistance. Hence, this project will avoid falling in what has been called as the potential new ‘Dark Middle Age” era of lack of antibiotics.Status
CLOSEDCall topic
MSCA-IF-2017Update Date
28-04-2024
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