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Research interests

The He lab focuses on understanding the evolution and structuring of population diversities in space and time via testable theoretical models. We integrate concepts and tools from population genetics, genomic evolution, and disease ecology, and develops new methodologies to answer questions regarding parasite-pathogen coevolution, rapid adaptation, and demographic histories.

 

Feel free to contact me if you are interested in joining my group. We are recruiting!

CURRENT FOCI

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An antigenic diversification threshold for falciparum malaria transmission at high endemicity

The vast diversity of the falciparum malaria parasite, as seen by the immune system of hosts in high transmission regions, underlies both high prevalence of asymptomatic infections and partial protection to re-infection despite previous exposure. This large antigenic diversity of the parasite challenges control and elimination efforts. We propose a threshold quantity for antigenic innovation, we call Rdiv, measuring the potential of transmission to accumulate new antigenic variants over time. When Rdiv is pushed below one by reduced transmission intensity, new genes encoding this variation can no longer accumulate, resulting in a lower number of strains and facilitating further intervention. This innovation number can be applied to other infectious diseases with fast turnover of antigens, where large standing diversity similarly opposes successful intervention.

Check it out at PLoS Computational Biology.

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Collaboration: Quantifying asymptomatic infection and transmission of COVID-19

As health officials face another wave of COVID-19, they require estimates of the proportion of infected cases that develop symptoms, and the extent to which symptomatic and asymptomatic cases contribute to community transmission. Recent asymptomatic testing guidelines are ambiguous. Using an epidemiological model that includes testing capacity, we show that many infections are nonsymptomatic but contribute substantially to community transmission in the aggregate. Their individual transmissibility remains uncertain. If they transmit as well as symptomatic infections, the epidemic may spread at faster rates than current models often assume. If they do not, then each symptomatic case generates, on average, a higher number of secondary infections than typically assumed. Regardless, controlling transmission requires community-wide interventions informed by extensive, well-documented asymptomatic testing.

Check it out at PNAS.