Yi Hao CHAN 

BIOGRAPHY

Dr Yi-Hao Chan graduated from the National University of Singapore with a Degree in Biomedical Sciences. Following, he completed his PhD with the A*STAR Graduate Scholarship on immune pathogenesis of alphaviruses. He was then awarded the A*STAR International Fellowship to pursue his postdoctoral training in Rockefeller University in New York, USA, under the tutelage of Dr Jean-Laurent Casanova, working on neuron-intrinsic antiviral factors and monogenic disorders that predispose patients to childhood Herpes Simplex Encephalitis (HSE) and isolated SARS-CoV-2 Encephalitis. He reported human TMEFF1 as the first discovered HSV-1 restriction factor in the brain in Nature. He also reported DBR1 deficiency as a genetic etiology of isolated SARS-CoV-2 brainstem encephalitis in Journal of Experimental Medicine. He co-authored multiple studies on inborn errors of immunity underlying multisystem inflammation syndrome in children (MIS-C), Mendelian susceptibility to mycobacterial disease (MSMD) and HSE, published in Science, Cell, and Science Immunology. He was awarded the RUCCTS pilot grant from the Shapiro-Silverberg Fund for the Advancement of Translational Research. He was also awarded the A*STAR Young Achiever in 2023 for his stellar academic achievements. He is also an Associate Editor for the Viral Immunology section at Frontiers in Immunology and is on the editorial board for the Journal of Human Immunology. In 2024, he joined A*STAR Infectious Diseases Labs to lead the efforts to study genetic and immunological determinants of life-threatening viral diseases.  

RESEARCH FOCUS

The Genetics of Host Immunity lab is interested in identifying and characterizing genetic and immunological determinants of life-threatening viral diseases, like arboviral encephalitis, or atopic dermatitis eczema herpeticum. Our research focusses on assessing rare, germline monogenic inborn errors of immunity, which are identified by WES or WGS, that can affect cell-intrinsic or host immune responses against viral infection. We are also interested in the presence of neutralizing autoantibodies against type-I interferons that can impede acute host immune responses against viral infections or result in adverse reactions to attenuated live viral vaccines. Identifying the mechanistic basis of disease, sometimes in a single patient, can point in the direction that can reveal other genetic or immunological basis in other patients, and highlight non-redundant immune pathways that are indispensable in fighting off viral infection and pathogenesis.