Virulence evolution

2021 ◽  
pp. 353-388
Author(s):  
Paul Schmid-Hempel
Keyword(s):  
Evolutionary Theory ◽  
Side Effect ◽  
Genetic Relatedness ◽  
Serial Passage ◽  
Transmission Rates ◽  
Host Interaction ◽  
Virulence Evolution ◽  
Trade Offs ◽  
Evolution Of Virulence ◽  
Context Manipulation

Virulence (i.e. reduction of host fitness) results from the parasite–host interaction. It can be an unselected side effect or the result of short-sighted evolution. The evolutionary theory of virulence predicts virulence by the fitness advantages for the parasite. Thereby, trade-offs among virulence level and host recovery or transmission rates are critical. This process can lead to lower, higher, or intermediate virulence, depending on conditions. Vertical transmission generally selects for lower virulence, whereas co-infection tends to increase virulence levels, also depending on genetic relatedness among the parasites. The sensitivity framework more generally addresses virulence levels in different systems; in this context, manipulation by parasites can result in significant virulence effects, especially when avoiding clearance and when effects are delayed. Different vaccination mechanisms can modify the evolution of virulence. Besides, virulence can evolve within hosts; for example, adaptation to a particular host type with serial passage attenuates virulence on other hosts.

scholarly journals The three Ts of virulence evolution during zoonotic emergence

2021 ◽  
Vol 288 (1956) ◽  
pp. 20210900
Author(s):  
Elisa Visher ◽  
Claire Evensen ◽  
Sarah Guth ◽  
Edith Lai ◽  
Marina Norfolk ◽  
...  
Keyword(s):  
Infectious Disease ◽  
Time Scales ◽  
Evolutionary Theory ◽  
Transmission Rate ◽  
Trade Off ◽  
Transmission Rates ◽  
Zoonotic Pathogens ◽  
Virulence Evolution ◽  
Trade Offs ◽  
Considerable Confusion

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.

Parental Influence and Sexual Selection

2021 ◽  
pp. 154-170
Author(s):  
Menelaos Apostolou
Keyword(s):  
Sexual Selection ◽  
Opportunity Cost ◽  
Parental Influence ◽  
Genetic Relatedness ◽  
Parental Choice ◽  
Direct Control ◽  
Arranged Marriage ◽  
Human Species ◽  
Trade Offs ◽  
Selection Force

This chapter addresses how the genetic relatedness between parents and their children results in the two parties having converging as well as diverging interests. In the domain of mating, these interests, along with other factors such as the trade-offs inherent in mating, give rise to an opportunity cost of free mate choice: Parents have much to lose if they allow their children to exercise choice freely. This opportunity cost provides a strong incentive to parents to influence their children’s mate choices. In preindustrial societies, parents manage to exercise direct control, which is predominantly manifested in the institution of arranged marriage. In postindustrial societies, parents exercise influence indirectly through manipulation. Ultimately, parental influence over mating gives rise to a sexual selection force, namely parental choice, which may be unique to the human species.

scholarly journals Transient virulence of emerging pathogens

2009 ◽  
Vol 7 (46) ◽  
pp. 811-822 ◽  
Author(s):  
Benjamin M. Bolker ◽  
Arjun Nanda ◽  
Dharmini Shah
Keyword(s):  
Genetic Variance ◽  
Evolutionary Dynamics ◽  
Growth Conditions ◽  
Emerging Pathogens ◽  
Potential Significance ◽  
Phase Selection ◽  
Transmission Rates ◽  
Virulence Evolution ◽  
High Virulence ◽  
Highly Virulent

Should emerging pathogens be unusually virulent? If so, why? Existing theories of virulence evolution based on a tradeoff between high transmission rates and long infectious periods imply that epidemic growth conditions will select for higher virulence, possibly leading to a transient peak in virulence near the beginning of an epidemic. This transient selection could lead to high virulence in emerging pathogens. Using a simple model of the epidemiological and evolutionary dynamics of emerging pathogens, along with rough estimates of parameters for pathogens such as severe acute respiratory syndrome, West Nile virus and myxomatosis, we estimated the potential magnitude and timing of such transient virulence peaks. Pathogens that are moderately evolvable, highly transmissible, and highly virulent at equilibrium could briefly double their virulence during an epidemic; thus, epidemic-phase selection could contribute significantly to the virulence of emerging pathogens. In order to further assess the potential significance of this mechanism, we bring together data from the literature for the shapes of tradeoff curves for several pathogens (myxomatosis, HIV, and a parasite of Daphnia ) and the level of genetic variation for virulence for one (myxomatosis). We discuss the need for better data on tradeoff curves and genetic variance in order to evaluate the plausibility of various scenarios of virulence evolution.

scholarly journals Evolution of Virulence in Fusarium oxysporum f. sp. vasinfectum Using Serial Passage Assays Through Susceptible Cotton

2008 ◽  
Vol 98 (3) ◽  
pp. 296-303 ◽  
Author(s):  
B. Wang ◽  
C. L. Brubaker ◽  
W. Tate ◽  
M. J. Woods ◽  
J. J. Burdon
Keyword(s):  
Fusarium Oxysporum ◽  
Length Polymorphism ◽  
Fragment Length ◽  
Fragment Length Polymorphism ◽  
Rhizosphere Soil ◽  
Serial Passage ◽  
Clear Correlation ◽  
Spontaneous Mutations ◽  
Disease Symptoms ◽  
Evolution Of Virulence

Fifty strains of Fusarium oxysporum, recovered from rhizosphere soil around native Gossypium species and found to be mildly virulent on cotton (Gossypium hirsutum), were used to assay the propensity for evolution of virulence using serial passage assays through cotton. Only one lineage A strain, 2613, successfully completed 10 successive passages, while all others lost the ability to cause foliar disease symptoms at various stages during this process. Based on 46 amplified fragment length polymorphism (AFLP) markers generated with four EcoRI × MseI primer combinations, mutants were identified in offspring isolates from strain 2613 regardless of whether serial passages occurred in cotton or on water agar, suggesting the occurrence of spontaneous mutations. Significantly increased virulence was observed in the offspring isolates generated on cotton, while no increasing virulence was found in those obtained on water agar, suggesting that the evolution of virulence in F. oxysporum f. sp. vasinfectum is associated with the presence of cotton. No clear correlation was observed between the AFLP mutations and increased virulence in this study.

scholarly journals Evolution of virulence when transmission occurs before disease

2010 ◽  
Vol 6 (4) ◽  
pp. 505-508 ◽  
Author(s):  
Erik E. Osnas ◽  
Andrew P. Dobson
Keyword(s):  
Recovery Rate ◽  
Transition Rate ◽  
Transmission Rate ◽  
Evolutionarily Stable Strategy ◽  
Relative Difference ◽  
Stable Strategy ◽  
New Host ◽  
Virulence Evolution ◽  
Evolution Of Virulence ◽  
Evolutionarily Stable

Most models of virulence evolution assume that transmission and virulence are constant during an infection. In many viral (HIV and influenza), bacterial (TB) and prion (BSE and CWD) systems, disease-induced mortality occurs long after the host becomes infectious. Therefore, we constructed a model with two infected classes that differ in transmission rate and virulence in order to understand how the evolutionarily stable strategy (ESS) depends on the relative difference in transmission and virulence between classes, on the transition rate between classes and on the recovery rate from the second class. We find that ESS virulence decreases when expressed early in the infection or when transmission occurs late in an infection. When virulence occurred relatively equally in each class and there was disease recovery, ESS virulence increased with increased transition rate. In contrast, ESS virulence first increased and then decreased with transition rate when there was little virulence early in the infection and a rapid recovery rate. This model predicts that ESS virulence is highly dependent on the timing of transmission and pathology after infection; thus, pathogen evolution may either increase or decrease virulence after emergence in a new host.

scholarly journals Host heterogeneity mitigates virulence evolution

2020 ◽  
Vol 16 (1) ◽  
pp. 20190744 ◽  
Author(s):  
P. Signe White ◽  
Angela Choi ◽  
Rishika Pandey ◽  
Arthur Menezes ◽  
McKenna Penley ◽  
...  
Keyword(s):  
Experimental Evolution ◽  
Parasite Prevalence ◽  
Mixed Genotype ◽  
Selective Pressures ◽  
Virulence Evolution ◽  
Specific Host ◽  
Trade Offs ◽  
Evolutionary Trajectories ◽  
Parasite Populations ◽  
Host Heterogeneity

Parasites often infect genetically diverse host populations, and the evolutionary trajectories of parasite populations may be shaped by levels of host heterogeneity. Mixed genotype host populations, compared to homogeneous host populations, can reduce parasite prevalence and potentially reduce rates of parasite adaptation due to trade-offs associated with adapting to specific host genotypes. Here, we used experimental evolution to select for increased virulence in populations of the bacterial parasite Serratia marcescens exposed to either heterogeneous or homogeneous populations of Caenorhabditis elegans . We found that parasites exposed to heterogeneous host populations evolved significantly less virulence than parasites exposed to homogeneous host populations over several hundred bacterial generations. Thus, host heterogeneity impeded parasite adaptation to host populations. While we detected trade-offs in virulence evolution, parasite adaptation to two specific host genotypes also resulted in modestly increased virulence against the reciprocal host genotypes. These results suggest that parasite adaptation to heterogeneous host populations may be impeded by both trade-offs and a reduction in the efficacy of selection as different host genotypes exert different selective pressures on a parasite population.

scholarly journals Directional Gene Movement from Human-Pathogenic to Commensal-Like Streptococci

2001 ◽  
Vol 69 (8) ◽  
pp. 4858-4869 ◽  
Author(s):  
Awdhesh Kalia ◽  
Mark C. Enright ◽  
Brian G. Spratt ◽  
Debra E. Bessen
Keyword(s):  
Genetic Relatedness ◽  
Human Subjects ◽  
Housekeeping Genes ◽  
Group A Streptococci ◽  
Highly Pathogenic ◽  
Evolution Of Virulence ◽  
Genotypic Analysis ◽  
History Of ◽  
Group A ◽  
Low Levels

ABSTRACT Group A streptococci (GAS) are highly pathogenic for humans, and their closest genetic relatives, group C and G streptococci (GCS and GGS, respectively), are generally regarded as commensals, although they can be found in association with human disease. As part of an effort to better understand the evolution of virulence, the phylogenetic relationships between GAS, GCS, and GGS were examined. The nucleotide sequence was determined for an internal portion of seven housekeeping (neutral) loci among >200 isolates of GAS and 34 isolates of GCS or GGS obtained from human subjects. Genotypic analysis failed to show support for the separation of GCS and GGS into two distinct populations. Unlike GAS, there was poor concordance betweenemm type and genetic relatedness among GCS and GGS. All housekeeping genes within GAS displayed relatively low levels of sequence diversity. In contrast, individual GCS and GGS strains had mosaic genomes, containing alleles at some loci that were similar or identical to GAS alleles, whereas the alleles at other loci were about 10 to 30% diverged. The data provide evidence for a history of recent interspecies transfer of neutral genes that exhibits a strong net directionality from GAS donors to GCS and GGS recipients. A model for the evolution of GAS and of GCS and GGS is described.

scholarly journals Modelling the evolution of viral oncogenesis

2019 ◽  
Vol 374 (1773) ◽  
pp. 20180302 ◽  
Author(s):  
Carmen Lía Murall ◽  
Samuel Alizon
Keyword(s):  
Life Histories ◽  
Viral Population ◽  
Oncogenic Viruses ◽  
Chronic Infections ◽  
Dna Viruses ◽  
Virulence Evolution ◽  
Trade Offs ◽  
Cell Life ◽  
Risk Of Cancer ◽  
Case Mortality

Most human oncogenic viruses share several characteristics, such as being DNA viruses, having long (co)evolutionary histories with their hosts and causing either latent or chronic infections. They can reach high prevalences while causing relatively low case mortality, which makes them quite fit according to virulence evolution theory. After analysing the life histories of DNA oncoviruses, we use a mathematical modelling approach to investigate how the virus life cycle may generate selective pressures favouring or acting against oncogenesis at the within-host or at the between-host level. In particular, we focus on two oncoprotein activities, namely extending cell life expectancy and increasing cell proliferation rate. These have immediate benefits (increasing viral population size) but can be associated with fitness costs at the epidemiological level (increasing recovery rate or risk of cancer) thus creating evolutionary trade-offs. We interpret the results of our nested model in light of the biological features and identify future perspectives for modelling oncovirus dynamics and evolution. This article is part of the theme issue ‘Silent cancer agents: multi-disciplinary modelling of human DNA oncoviruses’.

scholarly journals An Analysis of Host Adaptation and Its Relationship with Virulence in Cucumber mosaic virus

2005 ◽  
Vol 95 (7) ◽  
pp. 827-833 ◽  
Author(s):  
Soledad Sacristán ◽  
Aurora Fraile ◽  
José M. Malpica ◽  
Fernando García-Arenal
Keyword(s):  
Cucumber Mosaic Virus ◽  
Mosaic Virus ◽  
Experimental Evolution ◽  
Host Adaptation ◽  
Trade Offs ◽  
Evolution Of Virulence ◽  
Host Growth ◽  
Before And After ◽  
Pathogen Populations ◽  
The Relationship

The host range of a pathogen can have special consequences on its evolution and the evolution of its virulence. For generalists, adaptation to different hosts may be conditioned by different trade-offs in the pathogen's life history and be affected by evolutionary processes that shape pathogen populations. We have examined adaptation of Cucumber mosaic virus (CMV) to different hosts, and analyzed the relationship between host adaptation and virulence. For this, six CMV isolates from central Spain from three different hosts were compared for the ability to multiply and to affect host growth. These analyses were done before and after an experimental evolution process consisting of 10 serial passages in the original host of the isolate. The differential capacity to infect different hosts was compatible with host adaptation. However, the capacity to multiply in different hosts did not provide evidence of host adaptation and was not improved after 10 passages, suggesting that fitness of the natural population of CMV was at, or near to, its maximum. No relationship was found between capacity of multiplication and virulence in any of the three different hosts. These results suggest that the “trade-off” model for the evolution of virulence may not apply to CMV.

scholarly journals Interplay between the cell envelope and mobile genetic elements shapes gene flow in populations of a nosocomial pathogen

2020 ◽  
Author(s):  
Matthieu Haudiquet ◽  
Amandine Buffet ◽  
Olaya Rendueles ◽  
Eduardo P.C. Rocha
Keyword(s):  
Gene Flow ◽  
Biosynthetic Pathway ◽  
Cell Envelope ◽  
Antibiotic Resistance Genes ◽  
Mobile Genetic Elements ◽  
Nosocomial Pathogen ◽  
Genetic Elements ◽  
Specific Phage ◽  
Trade Offs ◽  
Evolution Of Virulence

ABSTRACTMobile genetic elements (MGEs) drive genetic transfers between bacteria using mechanisms that are affected by the cell envelope composition, notably the capsule. Here, we show that capsules constrain phage-mediated gene flow between closely related serotypes in Klebsiella pneumoniae, a high-priority nosocomial enterobacteria. Serotype-specific phage pressure may also explain the inactivation of capsule genes, which occur frequently and recapitulate the capsule biosynthetic pathway. We show that plasmid conjugation is increased upon capsule inactivation and that capsule re-acquisition leaves long recombination tracts around the capsular locus. This suggests that capsule inactivation by phage pressure facilitates its subsequent re-acquisition by conjugation, a process re-wiring gene flow towards novel lineages whenever it leads to serotype swaps. These results reveal the basis of trade-offs between the evolution of virulence and multidrug resistance. They also caution that some alternatives to antibiotic therapy may select for capsule inactivation, thus decreasing virulence but facilitating antibiotic resistance genes acquisition.

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