Ping Zhang

The maps of human genetic variation that associate with disease susceptibility allow us to generate and test biological hypotheses. Emerging evidence suggests that causal variants underlying disease susceptibility often function through regulatory effects on the transcription of target genes. However, there are challenges in harnessing of susceptibility loci for drug target identification and therapeutic application, including limitations in (i) exposition of causal variants within susceptibility loci, (ii) understanding of the context specificity, and (iii) mechanistic insights into their influence on cellular behaviours and clinical outcomes.

My current research is focused on identifying and characterising regulatory variants modulating extreme innate immune response phenotypes and the interplay of innate-adaptive immunity in order to gain insights into the causal mechanisms driving heterogeneity of pathogenesis in infectious diseases including sepsis, tuberculosis and COVID19. The research combines bioinformatics, multi-omics approaches and CRISPR-based epigenetic editings to study variants in disease relevant primary tissue/cells and human iPSC-derived models.