Defensive symbiosis and the evolution of virulence

Mapping Intimacies ◽

10.1101/422436 ◽

2018 ◽

Author(s):

Paul G. Nelson ◽

Georgiana May

Keyword(s):

Entire Range ◽

Direct Effects ◽

Continuous Trait ◽

Defensive Symbiosis ◽

Evolution Of Virulence ◽

Host Mortality ◽

Selection For ◽

Context Dependent ◽

Counterintuitive Result

AbstractAlthough environments rife with enemies should cause selection for defensive traits, such enemy-rich environments should also select for greater virulence in co-occurring symbionts, yet many defensive symbionts cause little to no damage while protecting their hosts from enemies. Thus, co-infection of a defensive symbiont and a parasite is predicted to select both for increased virulence in co-infecting symbionts and for increased defense in the protective symbiont. Why then do we observe defensive mutualists that protect hosts while causing little damage? To address this question, we build a symbiont-centered model that incorporates the evolution of two independent traits: defense and virulence. Virulence is modeled as a continuous trait spanning mutualism (negative virulence) and parasitism (virulence) and thus accounts for the entire range of direct effects that symbionts have on host mortality. Defense is modeled as a continuous trait that ameliorates the costs to the host associated with co-infection with a deleterious parasite. We obtain the counterintuitive result that the evolution of increased defense in one symbiont largely leads to the evolution of lower virulence in both symbionts and may even facilitate pathogens evolving to mutualism. However, results are context-dependent and when defensive traits are costly, the evolution of greater defense may also lead to higher virulence.

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Detection, not mortality, constrains the evolution of virulence

10.1101/2021.11.14.468516 ◽

2021 ◽

Author(s):

David A Kennedy

Keyword(s):

Mathematical Model ◽

Disease Severity ◽

Behavioral Change ◽

Scientific Literature ◽

Empirical Support ◽

Infectious Period ◽

Trade Off ◽

Evolution Of Virulence ◽

Host Mortality

Why would a pathogen evolve to kill its hosts when killing a host ends a pathogen's own opportunity for transmission? A vast body of scientific literature has attempted to answer this question using "trade-off theory," which posits that host mortality persists due to its cost being balanced by benefits of other traits that correlate with host mortality. The most commonly invoked trade-off is the mortality-transmission trade-off, where increasingly harmful pathogens are assumed to transmit at higher rates from hosts while the hosts are alive, but the pathogens truncate their infectious period by killing their hosts. Here I show that costs of mortality are too small to plausibly constrain the evolution of disease severity except in systems where survival is rare. I alternatively propose that disease severity can be much more readily constrained by a cost of behavioral change due to the detection of infection, whereby increasingly harmful pathogens have increasing likelihood of detection and behavioral change following detection, thereby limiting opportunities for transmission. Using a mathematical model, I show the conditions under which detection can limit disease severity. Ultimately, this argument may explain why empirical support for trade-off theory has been limited and mixed.

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Peer Review #1 of "Not always a matter of context: direct effects of red on arousal but context-dependent moderations on valence (v0.2)"

10.7287/peerj.2515v0.2/reviews/1 ◽

2016 ◽

Keyword(s):

Peer Review ◽

Direct Effects ◽

Context Dependent

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Relationship between litter size and perinatal and pre-weaning survival in pigs

Animal Science ◽

10.1017/s1357729800052383 ◽

2002 ◽

Vol 74 (2) ◽

pp. 217-222 ◽

Cited By ~ 59

Author(s):

M. S. Lund ◽

M. Puonti ◽

L. Rydhmer ◽

J. Jensen

Keyword(s):

Litter Size ◽

Negative Correlation ◽

Genetic Effects ◽

Direct Effects ◽

Selection For ◽

Heritability Estimates ◽

The Relationship ◽

Piglet Survival

AbstractThe objective of this study was to analyse the relationship between direct and maternal genetic effects on litter size and piglet survival. The analyses were performed on records from 26 564 Landrace litters and 15 103 Yorkshire litters from first parity dams in Finnish herds. The trivariate model fitted total number of piglets born, proportion alive at birth and proportion survived from birth until 3 weeks as traits of the litter. The model included direct genetic and maternal genetic effects for all traits. In Landrace pigs, maternal heritabilities were estimated to be 0·11 for total number born, 0·06 for proportion alive at birth, and 0·08 for proportion survived from birth until 3 weeks. The corresponding estimates for the Yorkshire breed were 0·14, 0·06 and 0·01. All heritability estimates of direct effects were below 0·05. In the Landrace breed, there was a negative correlation of -0·39 between maternal genetic effects on total number born and maternal genetic effects on proportion survived from birth until 3 weeks and a negative correlation of -0·41 between direct and maternal genetic effects on proportion survived from birth until 3 weeks. These correlations were not significant in the Yorkshire breed. The results show that selection for number born in total alone will lead to a deterioration in the maternal ability of sows. Selection for pre-weaning survival could be achieved by selecting on direct and maternal components jointly.

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Selection for relative brain size affects context-dependent male preference for, but not discrimination of, female body size in guppies

Journal of Experimental Biology ◽

10.1242/jeb.175240 ◽

2018 ◽

Vol 221 (12) ◽

pp. jeb175240 ◽

Cited By ~ 12

Author(s):

Alberto Corral-López ◽

Alexander Kotrschal ◽

Niclas Kolm

Keyword(s):

Body Size ◽

Female Body ◽

Brain Size ◽

Male Preference ◽

Female Body Size ◽

Relative Brain Size ◽

Selection For ◽

Context Dependent

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Decline in Natural Fisheries — A Genetic Analysis and Suggestion for Recovery

Canadian Journal of Fisheries and Aquatic Sciences ◽

10.1139/f86-162 ◽

1986 ◽

Vol 43 (6) ◽

pp. 1298-1306 ◽

Cited By ~ 16

Author(s):

Giora W. Wohlfarth

Keyword(s):

Negative Selection ◽

Natural Waters ◽

Environmental Changes ◽

Monitoring Program ◽

Fish Populations ◽

Natural Environments ◽

Direct Effects ◽

Resident Population ◽

Selection For ◽

Bodies Of Water

Overfishing and pollution of the aquatic environment, in addition to their direct effects on natural fisheries, may have also influenced natural fish populations genetically. Overfishing drastically reduces population size and, since the larger individuals are selectively removed, is equivalent to selection for smaller sized fish. Adaptation of natural fish populations to their environment must have been reduced by rapid environmental changes resulting from pollution and infestation. Inbreeding, negative selection, and lack of adaption are here considered as the genetic causes for the decline of natural fisheries and lack of recovery. Restocking programs involving hatchery stocks are unlikely to solve this problem, since these stocks were selected for adaptation to hatchery environments and not to natural environments. A series of studies have demonstrated heterosis of interstrain crossbreds, mainly between hatchery and wild stocks of salmonids, for performance in natural waters. Two strategies could be implemented in restocking programs: stocking spawners of a domestic strain (preferably of one sex) for interbreeding with the resident population or direct stocking of crossbred fry. This should be tested in small isolated bodies of water and needs to be accompanied by a monitoring program in order to evaluate the results and minimize hazards.

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Effect of Low Concentrations of Prostacyclin on Platelet Function in Vitro

Anaesthesia and Intensive Care ◽

10.1177/0310057x9702500402 ◽

1997 ◽

Vol 25 (4) ◽

pp. 343-346 ◽

Cited By ~ 13

Author(s):

P. V. Van Heerden ◽

N. M. Gibbs ◽

N. Michalopoulos

Keyword(s):

Platelet Aggregation ◽

Entire Range ◽

Venous Blood ◽

Maximum Amplitude ◽

Adenosine Diphosphate ◽

Systemic Circulation ◽

Direct Effects ◽

Low Concentrations ◽

Platelet Aggregation Defect

The study was performed to determine the possible direct effects of low concentrations of prostacyclin that might spill over into the systemic circulation during the administration of inhaled aerosolized prostacyclin. Platelet aggregation in response to adenosine diphosphate and collagen, as well as measurement of the maximum amplitude of the thrombelastograph (TEG), was undertaken in vitro using venous blood exposed to low concentrations of prostacyclin (0, 10, 100 and 500 pg/ml) from eight healthy volunteers. There were statistically significant reductions in parameters of platelet aggregation in response to the agonists adenosine diphosphate (1 μmol/l and 8 μmol/l) and collagen (10 μmol/l) following exposure to as little as 10 pg/ml of prostacyclin. The maximum amplitude of the TEG was unchanged over the entire range of prostacyclin concentrations studied. The results indicate that low concentrations of prostacyclin or prostacyclin metabolite such as may be observed during inhaled aerosolized prostacyclin therapy are likely to be associated with a marked platelet aggregation defect. This defect was not detected by the TEG.

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