Daniel Zinder, Postdoctoral Researcher (2016-2017)



(773) 795-0960

205 Erman Hall
1103 E 57th St‎.
Chicago, IL 60637

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My current research focuses on the evolutionary, competitive and ecological dynamics that shape B-cells and antibody repertoires in response to repeated infection challenges. I am also interested in the study of the mechanisms that shape the antigenic and genetic diversity of various pathogens such as influenza, rotavirus and Pf. malaria. In my work, I use models of population transmission dynamics and inference techniques to identify the mechanisms driving evolutionary changes in these pathogens. Although vaccines against all of these pathogens exist, they are far from perfect. Why are vaccines against rotavirus not as effective in different parts of the world? How antigenically homogenous is Pf. malaria? Are influenza epidemics driven by antigenic novelty or by an increase in the susceptible pool? What prevents us from forming a broadly protective immune response against influenza? These are some of the questions I attempt to answer in my research. A better understanding of the principles governing antigenic diversification in pathogens and the principles that shape the immune response against them may help in the design of more effective interventions.


Zinder, D., Riolo A. M., Woods R. J. Pascual M. 2017. Role of competition in the strain structure of rotavirus under invasion and reassortment. bioRxiv.

Zinder, D., Rorick, M. M., Tiedje, K. E., Ruybal-Pesantez, S., Day, K. P., & Pascual, M. 2017. Conservation of single amino-acid polymorphisms in Plasmodium falciparum erythrocyte membrane protein 1 and association with severe pathophysiology. bioRxiv.


Zinder D., Bedford, T., Gupta, S. & Pascual, M. 2013. The roles of competition and mutation in shaping antigenic and genetic diversity in influenza. PLoS Pathogens, 9(1): e1003104.

Zinder D., Bedford, T., Baskerville, E.B., Woods, R.J., Roy, M. & Pascual, M. 2014. Seasonality in the migration and establishment of H3N2 influenza lineages with epidemic growth and decline. BMC Evolutionary Biology; 14:272.