The Conundrum of Relapse in STAT-C Therapy: Does HCV Play the Red Queen or Rip Van Winkle?

2011 ◽  
Vol 31 (04) ◽  
pp. 410-419 ◽  
Author(s):  
Robert Ralston ◽  
Ira Jacobson ◽  
Margaret Scull
1983 ◽  
Vol 40 (3) ◽  
pp. 189-189
Author(s):  
L. Scheinberg
Keyword(s):  

2010 ◽  
Vol 24 (3) ◽  
pp. 541-553 ◽  
Author(s):  
F. ÚBEDA ◽  
J. F. WILKINS

2005 ◽  
Vol 115 (504) ◽  
pp. F211-F224 ◽  
Author(s):  
Arthur J Robson

2018 ◽  
Author(s):  
Elizabeth L. Anzia ◽  
Jomar F. Rabajante

AbstractWinnerless coevolution of hosts and parasites could exhibit Red Queen dynamics, which is characterized by parasite-driven cyclic switching of expressed host phenotypes. We hypothesize that the application of antibiotics to suppress the reproduction of parasites can provide opportunity for the hosts to escape such winnerless coevolution. Here, we formulate a minimal mathematical model of host-parasite interaction involving multiple host phenotypes that are targeted by adapting parasites. Our model predicts the levels of antibiotic effectiveness that can steer the parasite-driven cyclic switching of host phenotypes (heteroclinic oscillations) to a stable equilibrium of host survival. Our simulations show that uninterrupted application of antibiotic with high-level effectiveness (> 85%) is needed to escape the Red Queen dynamics. Intermittent and low level of antibiotic effectiveness are indeed useless to stop host-parasite coevolution. This study can be a guide in designing good practices and protocols to minimize risk of further progression of parasitic infections.


2017 ◽  
Vol 372 (1736) ◽  
pp. 20160463 ◽  
Author(s):  
Thibault Latrille ◽  
Laurent Duret ◽  
Nicolas Lartillot

In humans and many other species, recombination events cluster in narrow and short-lived hot spots distributed across the genome, whose location is determined by the Zn-finger protein PRDM9. To explain these fast evolutionary dynamics, an intra-genomic Red Queen model has been proposed, based on the interplay between two antagonistic forces: biased gene conversion, mediated by double-strand breaks, resulting in hot-spot extinction, followed by positive selection favouring new PRDM9 alleles recognizing new sequence motifs. Thus far, however, this Red Queen model has not been formalized as a quantitative population-genetic model, fully accounting for the intricate interplay between biased gene conversion, mutation, selection, demography and genetic diversity at the PRDM9 locus. Here, we explore the population genetics of the Red Queen model of recombination. A Wright–Fisher simulator was implemented, allowing exploration of the behaviour of the model (mean equilibrium recombination rate, diversity at the PRDM9 locus or turnover rate) as a function of the parameters (effective population size, mutation and erosion rates). In a second step, analytical results based on self-consistent mean-field approximations were derived, reproducing the scaling relations observed in the simulations. Empirical fit of the model to current data from the mouse suggests both a high mutation rate at PRDM9 and strong biased gene conversion on its targets. This article is part of the themed issue ‘Evolutionary causes and consequences of recombination rate variation in sexual organisms’.


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