WITHIN-HOST PARASITE DYNAMICS, EMERGING TRADE-OFF, AND EVOLUTION OF VIRULENCE WITH IMMUNE SYSTEM

Infections by multiple genotypes are common in nature and are known to select for higher levels of virulence for some parasites. When parasites produce public goods (PGs) within the host, such co-infections have been predicted to select for lower levels of virulence. However, this prediction is based on simplifying assumptions regarding epidemiological feedbacks on the multiplicity of infections (MOI). Here, we analyse the case of parasites producing a PG (for example, siderophore-producing bacteria) using a nested model that ties together within-host and epidemiological processes. We find that the prediction that co-infection should select for less virulent strains for PG-producing parasites is only valid if both parasite transmission and virulence are linear functions of parasite density. If there is a trade-off relationship such that virulence increases more rapidly than transmission, or if virulence also depends on the total amount of PGs produced, then more complex relationships between virulence and the MOI are predicted. Our results reveal that explicitly taking into account the distribution of parasite strains among hosts could help better understand the selective pressures faced by parasites at the population level.

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A Bit of Sex Stabilizes Host–Parasite Dynamics

Journal of Theoretical Biology ◽

10.1006/jtbi.2001.2380 ◽

2001 ◽

Vol 212 (3) ◽

pp. 345-354 ◽

Cited By ~ 16

Author(s):

THOMAS FLATT ◽

NICOLAS MAIRE ◽

MICHAEL DOEBELI

Keyword(s):

Host Parasite ◽

Parasite Dynamics

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Host-parasite dynamics and the evolution of host immunity and parasite fecundity strategies

Bulletin of Mathematical Biology ◽

10.1007/bf02459459 ◽

1997 ◽

Vol 59 (3) ◽

pp. 427-450 ◽

Cited By ~ 19

Author(s):

Veijo Kaitala ◽

Mikko Heino ◽

Wayne M. Getz

Keyword(s):

Host Immunity ◽

Host Parasite ◽

Parasite Dynamics

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Salivarian Trypanosomes Have Adopted Intricate Host-Pathogen Interaction Mechanisms that Ensure Survival in Plain Sight of the Adaptive Immune System

Pathogens ◽

10.3390/pathogens10060679 ◽

2021 ◽

Vol 10 (6) ◽

pp. 679

Author(s):

Stefan Magez ◽

Joar Esteban Pinto Torres ◽

Seoyeon Oh ◽

Magdalena Radwanska

Keyword(s):

Immune System ◽

Trypanosoma Brucei ◽

Adaptive Immune System ◽

Sub Saharan Africa ◽

Survival Strategies ◽

Mechanical Transmission ◽

Sub Saharan ◽

Animal Trypanosomiasis ◽

Host Parasite ◽

Treatment And Diagnosis

Salivarian trypanosomes are extracellular parasites affecting humans, livestock and game animals. Trypanosoma brucei rhodesiense and Trypanosoma brucei gambiense are human infective sub-species of T. brucei causing human African trypanosomiasis (HAT—sleeping sickness). The related T. b. brucei parasite lacks the resistance to survive in human serum, and only inflicts animal infections. Animal trypanosomiasis (AT) is not restricted to Africa, but is present on all continents. T. congolense and T. vivax are the most widespread pathogenic trypanosomes in sub-Saharan Africa. Through mechanical transmission, T. vivax has also been introduced into South America. T. evansi is a unique animal trypanosome that is found in vast territories around the world and can cause atypical human trypanosomiasis (aHT). All salivarian trypanosomes are well adapted to survival inside the host’s immune system. This is not a hostile environment for these parasites, but the place where they thrive. Here we provide an overview of the latest insights into the host-parasite interaction and the unique survival strategies that allow trypanosomes to outsmart the immune system. In addition, we review new developments in treatment and diagnosis as well as the issues that have hampered the development of field-applicable anti-trypanosome vaccines for the implementation of sustainable disease control.

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Parasite variation and the evolution of virulence in a Daphnia-microparasite system

Parasitology ◽

10.1017/s0031182007003939 ◽

2007 ◽

Vol 135 (3) ◽

pp. 303-308 ◽

Cited By ~ 23

Author(s):

T. J. LITTLE ◽

W. CHADWICK ◽

K. WATT

Keyword(s):

Genetic Variation ◽

Rank Order ◽

Genetic Relationships ◽

Natural Populations ◽

Host Genotype ◽

Relative Growth ◽

Trade Off ◽

Relative Growth Rates ◽

Pasteuria Ramosa ◽

Evolution Of Virulence

SUMMARYUnderstanding genetic relationships amongst the life-history traits of parasites is crucial for testing hypotheses on the evolution of virulence. This study therefore examined variation between parasite isolates (the bacterium Pasteuria ramosa) from the crustacean Daphnia magna. From a single wild-caught infected host we obtained 2 P. ramosa isolates that differed substantially in the mortality they caused. Surprisingly, the isolate causing higher early mortality was, on average, less successful at establishing infections and had a slower growth rate within hosts. The observation that within-host replication rate was negatively correlated with mortality could violate a central assumption of the trade-off hypothesis for the evolution of virulence, but we discuss a number of caveats which caution against premature rejection of the trade-off hypothesis. We sought to test if the characteristics of these parasite isolates were constant across host genotypes in a second experiment that included 2 Daphnia host clones. The relative growth rates of the two parasite isolates did indeed depend on the host genotype (although the rank order did not change). We suggest that testing evolutionary hypotheses for virulence may require substantial sampling of both host and parasite genetic variation, and discuss how selection for virulence may change with the epidemiological state of natural populations and how this can promote genetic variation for 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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How host phenology impacts multi-season epidemic cycles

10.1101/2021.06.07.447391 ◽

2021 ◽

Author(s):

Hannelore MacDonald ◽

Dustin Brisson

Keyword(s):

Mathematical Model ◽

Population Dynamics ◽

Population Cycles ◽

Seasonal Activity ◽

Host Interactions ◽

Host Phenology ◽

Demographic Impact ◽

Host Parasite ◽

Parasite Populations ◽

Parasite Dynamics

Parasite-host interactions can result in periodic population dynamics when parasites over-exploit host populations. The timing of host seasonal activity, or host phenology, determines the frequency and demographic impact of parasite-host interactions which may govern if the parasite can sufficiently over-exploit their hosts to drive population cycles. We describe a mathematical model of a monocyclic, obligate-killer parasite system with seasonal host activity to investigate the consequences of host phenology on host-parasite dynamics. The results suggest that parasites can reach the densities necessary to destabilize host dynamics and drive cycling in only some phenological scenarios, such as environments with short seasons and synchronous host emergence. Further, only parasite lineages that are sufficiently adapted to phenological scenarios with short seasons and synchronous host emergence can achieve the densities necessary to over-exploit hosts and produce population cycles. Host-parasite cycles can also generate an eco-evolutionary feedback that slows parasite adaptation to the phenological environment as rare advantageous phenotypes are driven to extinction when introduced in phases of the cycle where host populations are small and parasite populations are large. The results demonstrate that seasonal environments can drive population cycling in a restricted set of phenological patterns and provides further evidence that the rate of adaptive evolution depends on underlying ecological dynamics.

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