What we do

HIV-pathogenesis with particular interest in understanding the mechanisms that enable some HIV-infected individuals to control the viral replication. These individuals are defined as long-term non-progressors (LTNPs) or elite controllers. Unveiling host factors and immune responses for such phenomenon will likely provide insight for the development of novel therapeutic interventions and more rational design for therapeutic vaccine components and functional cures.

To map the mechanism(s) and pathways of cytotoxic T lymphocytes (CTLs) exhaustion in chronic conditions such as viral infections and cancer. In particular my laboratory focuses on the role of immune checkpoints in deteriorating CTL function and exhaustion. We aim to better understand CTL exhaustion in order to develop novel immunotherapies against chronic infections and cancer.

Our team works on breast cancer, colorectal, lung, melanoma, viral-associated cancers and hematological cancers.

The team’s findings fundamentally have changed how we look at neonatal susceptibility to infection by suggesting it is caused by active immune suppression during this developmental period, as opposed to the immaturity of immune cells. This discovery highlights the critical role of temporal immune suppression to allow swift adaptation of microbial communities in the gut of newborns. Thus, our team works on understanding the cross-talk between the immune system and the microbiome.

Our team works to understand why a subset of infected individuals with SARS-CoV-2 experience long-COVID. In particular, those who exhibit the most debilitating symptoms Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). A serious illness that affects multiple body systems. Our team is interested in identifying targetable mechanisms for the development of treatments against ME/CFS.