Contact information
Juthathip Mongkolsapaya
Professor and Associate Research Fellow
Our main research is to understand immune-responses, particularly antibody responses, against emerging pathogens, such as dengue virus, zika virus, HIV, Ebola virus, SARS and MERS and, the most recent, SARS-CoV2. We employ a wide range of approaches including virology, immunology, biochemistry, and structural biology to elucidate pathogenic mechanisms, to generate diagnostic and therapeutic reagents, design vaccines, and contributed to policy development. For example, during the COVID pandemic, we generated reagents that were involved in establishing a protocol to measure the antibody response, which have been used to monitoring the immune status in UK population. Hundreds of monoclonal antibodies were generated and characterised for their neutralisation activities, cross-reaction among the variants, and bio-physical properties. And in combination with crystal and cryo-EM structures, we described the antigenic distance among the variants and how new emerging variants escaped from existing immunity.
I am a CAMS Oxford Institute (COI) PI and am now based at the Mahidol Oxford Research Unit (MORU) in Bangkok. This is one of the overseas units of The Centre for Tropical Medicine and Global Health
Recent publications
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Concerted deletions eliminate a neutralizing supersite in SARS-CoV-2 BA.2.87.1 spike.
Duyvesteyn HME. et al, (2024), Structure (London, England : 1993), 32, 1594 - 1602.e6
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Immunogenicity of Abdala COVID-19 vaccine in Vietnamese people after primary and booster vaccinations: A prospective observational study in Vietnam
Thanh TT. et al, (2024), International Journal of Infectious Diseases, 147, 107173 - 107173
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Oligomerization-driven avidity correlates with SARS-CoV-2 cellular binding and inhibition
(2024), Proceedings of the National Academy of Sciences, 121
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A structure-function analysis shows SARS-CoV-2 BA.2.86 balances antibody escape and ACE2 affinity
Liu C. et al, (2024), Cell Reports Medicine, 5, 101553 - 101553
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Emerging variants develop total escape from potent monoclonal antibodies induced by BA.4/5 infection.
Liu C. et al, (2024), Nature communications, 15