Draft:Vinod Balasubramaniam

Postdoctoral training at Mount Sinai

From 2014 to 2017, Balasubramaniam undertook postdoctoral training in the laboratory of Professor Adolfo García-Sastre at the Department of Microbiology, Icahn School of Medicine at Mount Sinai in New York City. García-Sastre is a Howard Hughes Medical Institute investigator and one of the world's foremost influenza and emerging virus researchers.^[1][3] During this period, Balasubramaniam contributed to several high-impact studies on flavivirus–host interactions and innate immune evasion, including work published in Cell Host & Microbe, PLOS Pathogens, Nature Microbiology, and Cell.^[4][5][6][7]

Monash University Malaysia

After completing his postdoctoral training, Balasubramaniam returned to the Jeffrey Cheah School of Medicine and Health Sciences at Monash University Malaysia, initially as a Senior Lecturer (2017–2023) before being promoted to Associate Professor in 2023.^[1][2] He was appointed Head of the Infection and Immunity Research Strength, where he leads a multidisciplinary team of postdoctoral researchers and PhD students.^[2]

He has supervised 16 PhD students (9 completed, 7 ongoing), as well as BMedSci Honours students, and coordinates the Young Scholar Program (YSP), a flagship research internship for pre-medical students at the School.^[1]

Flavivirus immune evasion and STAT2 degradation

Balasubramaniam was a co-author on a 2016 study published in Cell Host & Microbe that demonstrated Zika virus targets the human STAT2 protein for proteasomal degradation via its NS5 protein, thereby inhibiting type I interferon signalling. The study showed this mechanism was species-specific to human cells, helping to explain why immunocompetent mouse models failed to recapitulate Zika disease.^[4]

He subsequently co-authored a 2017 study in PLOS Pathogens that established Stat2 knockout mice as a novel animal model for Zika virus pathogenesis, demonstrating for the first time that these mice were highly susceptible to ZIKV infection and revealing strain-specific differences in virulence between African and Asian ZIKV lineages.^[5]

Flavivirus–host protein interactomics

In 2018, Balasubramaniam contributed to a comparative flavivirus–host protein interaction mapping study published in Cell, a collaboration led by Professor Nevan Krogan's laboratory at the University of California, San Francisco (UCSF). The study generated the first whole-genome interactomics map of Zika and dengue virus interactions with human proteins, revealing that flavivirus NS5 suppresses interferon-stimulated genes via the PAF1C transcription complex, and that chemical manipulation of the SEC61 translocon inhibits replication of both DENV and ZIKV in human and mosquito cells.^[6]

RIG-I signalling and KHSRP

Through a systems-based analysis of RIG-I-dependent signalling published in Nature Microbiology (2017), Balasubramaniam was also involved in the identification of KHSRP as an inhibitor of RIG-I receptor activation, providing novel targets for host-directed antiviral strategies.^[7]

Zika virus neurotropism and brain organoid models

Balasubramaniam was involved in investigation of the molecular mechanisms of Zika virus-induced microcephaly, demonstrating that ZIKV infection modulates epigenetic DNA methylationpatterns in neural genes using brain organoid models, work published in mSystems (2018) in collaboration with the García-Sastre laboratory.^[8]

Antiviral drug repurposing and discovery

Balasubramaniam leads research into novel drug repurposing platforms using bioinformatics, molecular dynamics simulations, and in vitro validation. Key findings include the demonstration that zafirlukast, a leukotriene receptor antagonist, exhibits antiviral and immunomodulatory effects against flaviviruses via TNF signalling pathway inhibition,^[9] and that dichloroacetate (DCA) targeting glucose metabolism reduces Zika virus replication in brain cortical progenitors, the latter in collaboration with Professor William James at the University of Oxford.^[10]

Enterovirus research

His group investigates host factors involved in the neuropathogenesis of Enterovirus D68 (EV-D68) and Enterovirus A71 (EV-A71), employing whole-genome transcriptomics, multi-omics approaches, and identification of neutralising epitopes of monoclonal antibodies in EV-D68 antibody-escape mutants.^[1]