Adaptive immune memory response abrogates antibody boosting following vaccination Eugenia Z. Ong1,2, Esther S. Gan*1,2, Ruklanthi de Alwis*1,2, Limin Wijaya3, Xinmei Ong1,2, Menglan Zhang4, Abigail WL Wong3, Yin Bun Cheung5,6, Raphaël M. Zellweger1,2, Eng Eong Ooi1,2,7,8, Jenny G Low1,2,3, 1Viral Research and Experimental Medicine Centre @ Singhealth-Duke NUS; 2Programme in Emerging Infectious Diseases, Duke-NUS Medical School; 3Department of Infectious Diseases, Singapore General Hospital; 4Duke-NUS Medical School; 5Center for Quantitative Medicine, Duke-NUS Medical School; 6 Department for International Health, University of Tampere, 33100 Finland; 7Department of Microbiology and Immunology, Yong Loo Lin School of Medicine, National University of Singapore; 8Antimicrobial Resistance Interdisciplinary Research Group, Singapore-MIT Alliance for Research & Technology (SMART)
Waning immunity coupled with reduced vaccine uptake have lowered population herd immunity, thereby enabling re-emergence of vaccine-preventable diseases. Catch-up vaccination programs can boost antibody titers and restore herd immunity. We set out to define the baseline antibody titer that could benefit from catch-up measles, mumps and rubella (MMR) vaccination in healthcare workers. However, genome expression profiling coupled with MMR serology serendipitously revealed unexpected insights into antibody boosting. We measured antibody response and conducted whole blood genome expression profiling in subjects undergoing catch-up MMR vaccination before and at various time points post-vaccination. Despite seropositivity at baseline, antibody titer boosting was most common in rubella virus (RV) antibodies as compared to either measles or mumps following catch-up vaccination. This increase in antibody titers were associated with induction of innate immune and pro-inflammatory signaling following vaccination. Interestingly, similar trend in gene expression was observed in those seronegative for RV antibodies at baseline, which is consistent with previously reported findings on live vaccine infection. In contrast, genes associated with activation and proliferation of adaptive immune cells, which in our study were mostly related to T-cell activation and signaling, were induced only in those without antibody boosting. Our findings collectively suggest that adaptive immune memory response abrogates quantifiable rise in antibody titers, likely through prevention or termination of vaccine infection. Significant antibody boosting upon catch-up vaccination instead suggests insufficient immunity against infection. Our findings further suggest a practical approach to evaluate vaccine efficacy and estimate population herd immunity levels.
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