My research focuses on integrating approaches from evolutionary genomics, mathematical statistics, machine learning and computational biology to understand various evolutionary processes. I am particularly interested in investigating the relative contributions of stochastic and deterministic forces to evolutionary phenomena across three major research directions:
1. Adaptive evolution of viruses. I explore viruses such as SARS-CoV-2, IBV, and PEDV to understand their adaptive evolution, including factors such as origin, cross-species transmission, intra- and inter-host evolution, and spread dynamics of emerging variants. This research direction contributes to my understanding of viral evolution and its implications for public health.
2. Theoretical aspects of traditional evolutionary processes. I delve into theoretical aspects of traditional evolutionary processes by combining evolutionary approaches with mathematical modeling, machine learning, and computational simulation. By analyzing publicly available data, I aim to understand various aspects of evolution, including mutation rate, individual-based genetic drift, epistasis, fitness landscapes, and Hill-Robertson effect. This interdisciplinary approach helps me uncover fundamental principles underlying evolutionary dynamics.
3. Genotype-phenotype prediction using AI. I utilize advanced machine learning techniques to predict viral phenotypes based on genome sequences. My research focuses on constructing models to accurately predict characteristics such as transmissibility, tissue tropism, and receptor binding capabilities of different viral strains. This approach aims to provide crucial data support for vaccine and drug development, enhancing public health preparedness.
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Ph.D. in Biochemistry and Molecular Biology, 2020
Sun Yat-sen University
B.S. in Biotechnology, 2015
Sun Yat-sen University
Research include:
Project on the evolution of SARS-CoV-2, including origin, transmission, adaptive evolution, etc.
This paper proposed a runaway model, applicable to both the germline and soma, whereby mutator mutations form a positive-feedback loop.
How many incoming travelers (I0 at time 0, equivalent to the ‘founders’ in evolutionary genetics) infected with SARS-CoV-2 who visit or return to a region could have started the epidemic of that region? I0 would be informative about the initiation and progression of epidemics. To obtain I0, we analyze the genetic divergence among viral populations of different regions. By applying the ‘individual-output’ model of genetic drift to the SARS-CoV-2 diversities, we obtain I0 <10, which could have been achieved by one infected traveler in a long-distance flight.The conclusion is robust regardless of the source population, the continuation of inputs (It for t>0) or the fitness of the variants.With such a tiny trickle of human movement igniting many outbreaks, the crucial stage of repressing an epidemic in any region should, therefore, be the very first sign of local contagion when positive cases first become identifiable.The implications of the highly ‘portable’ epidemics, including their early evolution prior to any outbreak, are explored in the companion study (Ruan et al., personal communication).