Herpesviruses live harmoniously within human hosts, yet sometimes things go wrong, and they start to contribute to the development of major diseases, including post-viral chronic illnesses like ME/CFS, long COVID, and other autoimmune diseases like Multiple sclerosis. Our lab aims to unravel the biological mechanisms that convert a friend to a foe and its consequences on the host cell. Using novel state-of-the-art latency models and modern innovative molecular biology approaches, we try to understand the early stages of host-virus interactions, using single-cell to multicellular organoids.

Our research concentrates on:

• deciphering the interplay between pathogens and host mitochondria responsible for innate immunity;
• investigating the role of infections in the development of inflammation and autoimmunity;
• identifying the genetic alterations and infection-mediated cell-specific changes in the host that lead to chronic post-viral diseases like ME/CFS and long COVID.

Our previous groundbreaking discoveries include characterization of the molecular mechanism of HHV-6 reactivation from the human telomere and identification of a latency-lytic molecular switch that regulates HHV-6 reactivation.

We:

• specialize in latency models of double-stranded DNA viruses like Herpesviruses and implement in vitro models in primary and continuous cells to understand the crosstalk between the host and the pathogen;
• use organoid models for a better understanding of intricate regulation of virus latency in vivo;
• focus on mitochondria and peroxisome biology using innovative reporter proteins and advanced microscopy.
• Use co-infection models like Chlamydia and HHV-6 to understand human pathology.

Our downstream analytic capabilities include:

• Single-cell sequencing;
• Cross-disciplinary infection models;
• advanced microscopy;
• Anti-microbial drug designing.