Do persistent RNA viruses fit the trade-off hypothesis of virulence evolution?

2012 ◽  
Vol 2 (5) ◽  
pp. 556-560 ◽  
Author(s):  
Luis M Márquez ◽  
Marilyn J Roossinck
2015 ◽  
Vol 282 (1798) ◽  
pp. 20141069 ◽  
Author(s):  
Carmen Lía Murall ◽  
Chris T. Bauch ◽  
Troy Day

The human papillomavirus (HPV) vaccines hold great promise for preventing several cancers caused by HPV infections. Yet little attention has been given to whether HPV could respond evolutionarily to the new selection pressures imposed on it by the novel immunity response created by the vaccine. Here, we present and theoretically validate a mechanism by which the vaccine alters the transmission–recovery trade-off that constrains HPV's virulence such that higher oncogene expression is favoured. With a high oncogene expression strategy, the virus is able to increase its viral load and infected cell population before clearance by the vaccine, thus improving its chances of transmission. This new rapid cell-proliferation strategy is able to circulate between hosts with medium to high turnover rates of sexual partners. We also discuss the importance of better quantifying the duration of challenge infections and the degree to which a vaccinated host can shed virus. The generality of the models presented here suggests a wider applicability of this mechanism, and thus highlights the need to investigate viral oncogenicity from an evolutionary perspective.


2012 ◽  
Vol 9 (74) ◽  
pp. 2244-2254 ◽  
Author(s):  
Samuel Ojosnegros ◽  
Edgar Delgado-Eckert ◽  
Niko Beerenwinkel

RNA viruses exist as genetically diverse populations displaying a range of virulence degrees. The evolution of virulence in viral populations is, however, poorly understood. On the basis of the experimental observation of an RNA virus clone in cell culture diversifying into two subpopulations of different virulence, we study the dynamics of mutating virus populations with varying virulence. We introduce a competition–colonization trade-off into standard mathematical models of intra-host viral infection. Colonizers are fast-spreading virulent strains, whereas the competitors are less-virulent variants but more successful within co-infected cells. We observe a two-step dynamics of the population. Early in the infection, the population is dominated by colonizers, which later are outcompeted by competitors. Our simulations suggest the existence of steady state in which all virulence classes coexist but are dominated by the most competitive ones. This equilibrium implies collective virulence attenuation in the population, in contrast to previous models predicting evolution of the population towards increased virulence.


1999 ◽  
Vol 266 (1417) ◽  
pp. 397-404 ◽  
Author(s):  
Sharon L. Messenger ◽  
Ian J. Molineux ◽  
J. J. Bull

2006 ◽  
Vol 274 (1607) ◽  
pp. 225-230 ◽  
Author(s):  
Victoria Furió ◽  
Andrés Moya ◽  
Rafael Sanjuán

Mutation rates should be governed by at least three evolutionary factors: the need for beneficial mutations, the benefit of minimizing the mutational load and the cost of replication fidelity. RNA viruses show high mutation rates compared with DNA micro-organisms, and recent findings suggest that the cost of fidelity might play a role in the evolution of increased mutation rates. Here, by analysing previously published data from HIV-1 reverse transcriptase in vitro assays, we show a trade-off between enzymatic accuracy and the maximum rate of polymerization, thus providing a biochemical basis for the fitness cost of fidelity in HIV-1. This trade-off seems to be related to inefficient extension of mispairs, which increases fidelity at the expense of the polymerization rate. Since in RNA viruses fast replication is critical for survival, this could impose a high cost of fidelity and favour the evolution of high mutation rates.


2021 ◽  
Author(s):  
Hannelore MacDonald ◽  
Erol Akçay ◽  
Dustin Brisson

1AbstractMechanistic trade-offs between transmission and virulence are the foundation of current theory on the evolution of parasite virulence. Empirical evidence supporting these trade-offs in natural systems remains elusive, suggesting other factors could drive virulence evolution in the absence of a mechanistic trade-off. Several ecological factors modulate the optimal virulence strategies predicted from mechanistic trade-off models but none have been sufficient to explain the intermediate virulence strategies observed in most natural systems. The timing of seasonal activities, or phenology, is a common factor that influences the types and impact of many ecological interactions but is rarely considered in virulence evolution studies. We develop a mathematical model of a disease system with seasonal host activity to study the evolutionary consequences of host phenology on parasite virulence. Seasonal host activity is sufficient to drive the evolution of intermediate parasite virulence in the absence of traditional mechanistic trade-offs. The optimal virulence strategy is determined by both the duration of the host activity period as well as the variation in the host emergence timing. Parasites with low virulence strategies are favored in environments with long host activity periods and in environments in which all hosts emerge synchronously. These results demonstrate that host phenology may be sufficient, in the absence of mechanistic trade-offs, to select for intermediate optimal virulence strategies in some natural systems.


2021 ◽  
Vol 288 (1956) ◽  
pp. 20210900
Author(s):  
Elisa Visher ◽  
Claire Evensen ◽  
Sarah Guth ◽  
Edith Lai ◽  
Marina Norfolk ◽  
...  

There is increasing interest in the role that evolution may play in current and future pandemics, but there is often also considerable confusion about the actual evolutionary predictions. This may be, in part, due to a historical separation of evolutionary and medical fields, but there is a large, somewhat nuanced body of evidence-supported theory on the evolution of infectious disease. In this review, we synthesize this evolutionary theory in order to provide a framework for clearer understanding of the key principles. Specifically, we discuss the selection acting on zoonotic pathogens' transmission rates and virulence at spillover and during emergence. We explain how the direction and strength of selection during epidemics of emerging zoonotic disease can be understood by a three Ts framework: trade-offs, transmission, and time scales. Virulence and transmission rate may trade-off, but transmission rate is likely to be favoured by selection early in emergence, particularly if maladapted zoonotic pathogens have ‘no-cost’ transmission rate improving mutations available to them. Additionally, the optimal virulence and transmission rates can shift with the time scale of the epidemic. Predicting pathogen evolution, therefore, depends on understanding both the trade-offs of transmission-improving mutations and the time scales of selection.


2010 ◽  
Vol 73 (8) ◽  
pp. 1881-1908 ◽  
Author(s):  
Edgar Delgado-Eckert ◽  
Samuel Ojosnegros ◽  
Niko Beerenwinkel

2010 ◽  
Vol 365 (1548) ◽  
pp. 1907-1918 ◽  
Author(s):  
R. Froissart ◽  
J. Doumayrou ◽  
F. Vuillaume ◽  
S. Alizon ◽  
Y. Michalakis

The adaptive hypothesis invoked to explain why parasites harm their hosts is known as the trade-off hypothesis, which states that increased parasite transmission comes at the cost of shorter infection duration. This correlation arises because both transmission and disease-induced mortality (i.e. virulence) are increasing functions of parasite within-host density. There is, however, a glaring lack of empirical data to support this hypothesis. Here, we review empirical investigations reporting to what extent within-host viral accumulation determines the transmission rate and the virulence of vector-borne plant viruses. Studies suggest that the correlation between within-plant viral accumulation and transmission rate of natural isolates is positive. Unfortunately, results on the correlation between viral accumulation and virulence are very scarce. We found only very few appropriate studies testing such a correlation, themselves limited by the fact that they use symptoms as a proxy for virulence and are based on very few viral genotypes. Overall, the available evidence does not allow us to confirm or refute the existence of a transmission–virulence trade-off for vector-borne plant viruses. We discuss the type of data that should be collected and how theoretical models can help us refine testable predictions of virulence evolution.


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