Vinod Kumar leads the immune-genetics and infectious disease research group in identifying the human genes and molecular mechanisms that regulate appropriate immune response to infections, and which may contribute to susceptibility to sepsis and other infectious diseases.

Infections have an enormous impact on human health. My team is interested in deciphering the genetic and molecular mechanisms in disease, particularly infectious diseases. By taking advantage of state-of-the-art technologies and simultaneously assessing genetics and multi-omics in the context of host-pathogen interaction (http://www.humanfunctionalgenomics.org/), we are discovering druggable pathways to treat infectious diseases and developing genetic and genomic biomarkers for precision medicine.

Sepsis, a heterogeneous disorder caused by infections

Sepsis is a major global health problem primarily caused by bacterial and fungal infections. It is a life-threatening disorder characterized by a dysregulated immune response and multi-organ dysfunction. Current strategies using a “one-size-fits-all” treatment approach for sepsis have failed because of the extreme heterogeneity in disease outcome. Factors such as host genetics, pathogens and environmental factors, as well as the unique interaction between these factors in every individual, may contribute to heterogeneity in sepsis. Understanding the impact of these complex interactions on the function of the relevant cell types is therefore crucial to delineating the molecular basis of heterogeneity in outcome.

To do this, we are currently performing systems genetic studies using both patient and population-based cohorts. In particular, we are investigating how genetically determined inter-individual differences in molecular responses to infections contribute to the heterogeneity of fungal and bacterial sepsis outcome. Dissecting the genetic basis of sepsis heterogeneity to infections is a major step towards novel patient-specific therapeutic strategies, which depend on a deep understanding of the molecular interactions between host and pathogens.