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  1. null (Ed.)
    The contributions of asymptomatic infections to herd immunity and community transmission are key to the resurgence and control of COVID-19, but are difficult to estimate using current models that ignore changes in testing capacity. Using a model that incorporates daily testing information fit to the case and serology data from New York City, we show that the proportion of symptomatic cases is low, ranging from 13 to 18%, and that the reproductive number may be larger than often assumed. Asymptomatic infections contribute substantially to herd immunity, and to community transmission together with presymptomatic ones. If asymptomatic infections transmit at similar rates as symptomatic ones, the overall reproductive number across all classes is larger than often assumed, with estimates ranging from 3.2 to 4.4. If they transmit poorly, then symptomatic cases have a larger reproductive number ranging from 3.9 to 8.1. Even in this regime, presymptomatic and asymptomatic cases together comprise at least 50% of the force of infection at the outbreak peak. We find no regimes in which all infection subpopulations have reproductive numbers lower than three. These findings elucidate the uncertainty that current case and serology data cannot resolve, despite consideration of different model structures. They also emphasize how temporal data on testing can reduce and better define this uncertainty, as we move forward through longer surveillance and second epidemic waves. Complementary information is required to determine the transmissibility of asymptomatic cases, which we discuss. Regardless, current assumptions about the basic reproductive number of severe acute respiratory syndrome coronavirus 2 (SARS-Cov-2) should be reconsidered. 
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  2. Abstract

    Although parasites are known to have various effects on their hosts, we know little about their role in the assembly of diversifying host populations. Using an experimental bacterium (Pseudomonas fluorescens SBW25)-bacteriophage (ϕ2) system, we show that earlier parasite arrival significantly reduced the repeatability of host diversification. Earlier parasite arrival amplified the priority effects associated with the stochastic emergence of novel SBW25 phenotypes, translating into greater historical contingency in SBW25 diversification. Our results highlight the important role of parasite-host interactions in driving host adaptive radiation.

     
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