High adaptability to the microenvironment of the human host is an absolute requirement of all microbes that cause human diseases. Successful pathogens such as, Plasmodium falciparum, Mycobacterium tuberculosis, HIV-1 or SARS-CoV-2, while very different in complexity, share the capacity to acquire resistance, avoid elimination by the immune system, replicate or persist within the host and transmit.

The evolutionary and adaptive mechanisms that potentiate their capacity to thrive in the hostile environment of the human host are also involved in the response to antimicrobial treatment expediting the emerge of resistance. These processes are tightly regulated at the level of the genome and epigenome of the pathogens following fundamental molecular biology principals. Understanding the evolution of human pathogens and the use of computation systems biology approaches based on ‘OMICS’ technologies and bioinformatics allows staying ahead of the curve regarding emerging and re-emerging threats posed by infectious disease with emphasis on the challenge of antimicrobial resistance.

Also, applying functional and experimental genetics, that includes the technological breakthroughs of genome editing and modulation of gene expression at the RNA level, the team focus on understanding how pathogen genetic variations impact biological function leading to a functional validation of relevant molecular targets and biomarkers. Most importantly, the seamless integration between evolutionary genomics and experimental genetics has the potential to provide comprehensive novel insights into microbial mechanisms of pathogenicity that might open new avenues toward the design of novel, specific and more effective diagnostic applications, and therapeutics interventions.