Biology subjects

Hvid, U.

Publications and source records attributed to Hvid, U..

3 recordsLinked to original sources

bioRxiv2026

Long-range seeding drives exponential growth in early respiratory viral infection

Respiratory viruses spread within the host through both local expansion and occasional long-range dissemination that seeds new infection foci. We present LEAP, an analytically tractable within-host model that captures this two-scale process by coupling local plaque growth to long-range seeding. The model reduces to an age-dependent branching process and yields a closed-form expression for the exponential growth rate during early infection. Using empirical data to parametrize the model, we find that productive dissemination requires only a small number of successful long-range seeding events per infected cell, with distinct values for SARS-CoV-2 and influenza A virus. LEAP further predicts that, in these well-adapted viruses, interferon-mediated restriction only weakly affects exponential growth, while remaining decisive for poorly adapted ones. More broadly, the model provides a flexible framework for experimentally testable predictions of early infection dynamics. Significance StatementRespiratory viral infection is an inherently spatial process, in which the virus must colonize large areas of the airways to optimize reproduction. Recent studies in animal models infected with influenza A or SARS-CoV-2 have documented long-range stochastic jumps of viral populations between distant regions of the respiratory tract. The emerging picture is one of two co-occurring spatial processes: slow, local plaque expansion and long-range seeding events that are rare but crucial to rapid colonization of the airways. We introduce LEAP (Lotka-Euler Airway Pathogen model), a simple mathematical within-host model that captures these two-scale dynamics by coupling local plaque growth to stochastic long-range seeding. Using LEAP, measurements from the petri dish can directly produce predictions of infection dynamics in the body.

immunology↗

bioRxiv2026

Stochasticity in viral infection and host response: A competition between speed and reliability

The early stages of viral infection constitute a race between viral proliferation and interferon (IFN)-mediated defenses. Recent experiments on single-cell viral kinetics have demonstrated a high degree of stochasticity in the timing of viral release, but how this shapes the competition between virus and host remains unclear. We formulate a stochastic spatial model to address the question of how variability in the release of viral progeny and IFN affect the early infection dynamics. The model distinguishes between two types of timing noise: stochasticity in the initiation of release, and variability in the secretion time of individual virions. Our key result is an asymmetry in how noise affects outcomes: For the virus, stochastic initiation accelerates expansion, while for the host, effective containment via IFN benefits from precisely timed responses. For the secreting states, we find that a broader secretion profile (higher variability in particle release times) is always advantageous. In all cases, we find that stochasticity in signal timing plays a huge/central role in the early infections states.

immunology↗

bioRxiv2024

Competitive advantages of secondary adsorption-triggered lysis inhibition for T-even phages

T-even bacteriophages are known to employ lysis inhibition (LIN), where the lysis of an infected host is delayed in response to secondary adsorptions. Upon the eventual burst of the host, significantly more phage progenies are released. Here, we analysed the competitive advantage of LIN using a mathematical model. In batch culture, LIN provides a bigger phage yield at the end of the growth where all the hosts are infected due to an exceeding number of phage particles and, in addition, gives a competitive advantage against LIN mutants with rapid lysis by letting them adsorb to already infected hosts in the LIN state. By simulating plaque formation in a spatially structured environment, we show that, while LIN phages will produce a smaller zone of clearance, the area over which the phages spread is actually comparable to those without LIN. The analysis suggests that LIN induced by secondary adsorption is favourable in terms of competition, both in spatially homogeneous and inhomogeneous environments. Author SummaryT-even bacteriophages can delay the lysis of their hosts when they detect more phages are adsorbing to the hosts, increasing the progeny production per host. Using a mathematical model, we provide a quantitative analysis of this strategys competitive advantages and disadvantages in different environments. The model predicts that phage adsorption to lysis-inhibited cells provides a significant competitive advantage to lysis-inhibiting phage against phages that quickly lyse the cells. We also find that secondary infection-triggered delay does not hinder the spreading of the phage in a lawn of uninfected cells, even though the apparent plaque size is small. The analysis suggests that lysis inhibition provides a robust competitive advantage for a virulent phage.

microbiology↗