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Biology subjects

Champredon, D.

Publications and source records attributed to Champredon, D..

4 recordsLinked to original sources

Variance in Variants: Propagating Genome Sequence Uncertainty into Phylogenetic Lineage Assignment

Genetic sequencing is subject to many different types of errors, but most analyses treat the resultant sequences as if they are known without error. Next generation sequencing methods rely on significantly larger numbers of reads than previous sequencing methods in exchange for a loss of accuracy in each individual read. Still, the coverage of such machines is imperfect and leaves uncertainty in many of the base calls. On top of this machine-level uncertainty, there is uncertainty induced by human error, such as errors in data entry or incorrect parameter settings. In this work, we demonstrate that the uncertainty in sequencing techniques will affect downstream analysis and propose a straightforward method to propagate the uncertainty. Our method uses a probabilistic matrix representation of individual sequences which incorporates base quality scores as a measure of uncertainty that naturally lead to resampling and replication as a framework for uncertainty propagation. With the matrix representation, resampling possible base calls according to quality scores provides a bootstrap- or prior distribution-like first step towards genetic analysis. Analyses based on these re-sampled sequences will include a more complete evaluation of the error involved in such analyses. We demonstrate our resampling method on SARS-CoV-2 data. The resampling procedures adds a linear computational cost to the analyses, but the large impact on the variance in downstream estimates makes it clear that ignoring this uncertainty may lead to overly confident conclusions. We show that SARS-CoV-2 lineage designations via Pangolin are much less certain than the bootstrap support reported by Pangolin would imply and the clock rate estimates for SARS-CoV-2 are much more variable than reported.

bioinformatics↗

Inferring generation-interval distributions from contact-tracing data

Generation intervals, defined as the time between when an individual is infected and when that individual infects another person, link two key quantities that describe an epidemic: the reproductive number, [Formula], and the rate of exponential growth, r. Generation intervals are often measured through contact tracing by identifying who infected whom. We study how observed intervals differ from \"intrinsic\" intervals that could be estimated by tracing individual-level infectiousness, and identify both spatial and temporal effects, including censoring (due to observation time), and the effects of susceptible depletion at various spatial scales. Early in an epidemic, we expect the variation in the observed generation intervals to be mainly driven by the censoring and the population structure near the source of disease spread; therefore, we predict that correcting observed intervals for the effect of temporal censoring but not for spatial effects will provide a spatially informed \"effective\" generation-interval distribution, which will correctly link r and [Formula]. We develop and test statistical methods for temporal corrections of generation intervals, and confirm our prediction using individual-based simulations on an empirical network.

ecology↗

Equivalence of the Erlang SEIR epidemic model and the renewal equation

Most compartmental epidemic models can be represented using the Euler-Lotka renewal equation (RE). The value of the RE is not widely appreciated in the epidemiological modelling community, perhaps because its equivalence to standard models has not been presented rigorously in non-trivial cases. Here, we provide analytical expressions for the intrinsic generation interval distribution that must be used in the RE in order to yield epidemic dynamics that are identical to those of the susceptible-exposed-infectious-recovered (SEIR) compartmental model with Erlang-distributed latent and infectious periods. This class of models includes the standard (exponentially-distributed) SIR and SEIR models as special cases.

epidemiology↗

Exploring how generation intervals link strength and speed of epidemics

Infectious-disease outbreaks are often characterized by the reproductive number and exponential rate of growth r. provides information about out-break control and predicted final size. Directly estimating is difficult, while r can often be estimated from incidence data. These quantities are linked by the generation interval - the time between when an individual is infected by an infector, and when that infector was infected. It is often infeasible to ob-tain the exact shape of a generation-interval distribution, and to understand how this shape affects estimates of . We show that estimating generation interval mean and variance provides insight into the relationship between and r. We use examples based on Ebola, rabies and measles to explore approximations based on gamma-distributed generation intervals, and find that use of these simple approximations are often sufficient to capture the r- relationship and provide robust estimates of .

epidemiology↗