Evidence map›Paper›PMID 39799993›Full record

ArticleJournal of theoretical biology2025

Design, optimization, and inference of biphasic decay of infectious virus particles.

Jérémy Seurat, Krista R Gerbino, Justin R Meyer, Joshua M Borin, Joshua S Weitz

Abstract read
In one paragraph

Article in Journal of theoretical biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Article
  2. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors.

Jérémy SeuratInstitut de Biologie, Ecole Normale Superieure, Paris, 75005, France; School of Biological Sciences, Georgia Institute of Technology, Atlanta, 30332, GA, USA.
Krista R GerbinoDivision of Biological Sciences, University of California San Diego, La Jolla, 92093, CA, USA.
Justin R MeyerDivision of Biological Sciences, University of California San Diego, La Jolla, 92093, CA, USA.
Joshua M BorinDivision of Biological Sciences, University of California San Diego, La Jolla, 92093, CA, USA.
Joshua S WeitzInstitut de Biologie, Ecole Normale Superieure, Paris, 75005, France; School of Biological Sciences, Georgia Institute of Technology, Atlanta, 30332, GA, USA; Department of Biology, University of Maryland, College Park, 20742, MD, USA. Electronic address: jsweitz@umd.edu.

Funding

GENETIC MECHANISMS AND REGULATIONT32GM007240 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI HAMPTON, RANDOLPH Y. · 1985 to 2019
$23.8M
Synergistic control of acute respiratory pathogens by bacteriophage and the innate immune responseR01AI146592 · NIAID · UNIV OF MARYLAND, COLLEGE PARK · PI DEBARBIEUX, LAURENT, WEITZ, JOSHUA · 2019 to 2023
$2.4M
NIAID NIH HHS R01 AI146592NIGMS NIH HHS T32 GM007240
6 · The paper itself

Abstract

Virus population dynamics are driven by counter-balancing forces of production and loss. Whereas viral production arises from complex interactions with susceptible hosts, the loss of infectious virus particles is often approximated as a first-order kinetic process. As such, experimental protocols to measure infectious virus loss are not typically designed to identify non-exponential decay processes. Here, we propose methods to evaluate if an experimental design is adequate to identify multiphasic virus particle decay and to optimize the sampling times of decay experiments, accounting for uncertainties in viral kinetics. First, we evaluate synthetic scenarios of biphasic decays, with varying decay rates and initial proportions of subpopulations. We show that robust inference of multiphasic decay is more likely when the faster decaying subpopulation predominates insofar as early samples are taken to resolve the faster decay rate. Moreover, design optimization involving non-equal spacing between observations increases the precision of estimation while reducing the number of samples. We then apply these methods to infer multiple decay rates associated with the decay of bacteriophage ('phage') ΦD9, an evolved isolate derived from phage Φ21. A pilot experiment confirmed that ΦD9 decay is multiphasic, but was unable to resolve the rate or proportion of the fast decaying subpopulation(s). We then applied a Fisher information matrix-based design optimization method to propose non-equally spaced sampling times. Using this strategy, we were able to robustly estimate multiple decay rates and the size of the respective subpopulations. Notably, we conclude that the vast majority (94%) of the phage ΦD9 population decays at a rate 16-fold higher than the slow decaying population. Altogether, these results provide both a rationale and a practical approach to quantitatively estimate heterogeneity in viral decay.

Indexed as

BacteriophagesModels, BiologicalVirionKineticsFisher information matrixInferenceMultiphasic decayOptimal designViral decay

Identifiers

PMID39799993
PMCPMC12497359

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.