Natural Selection Associated With Infectious Diseases

2017 ◽  
pp. 177-191 ◽  
Author(s):  
M. Fumagalli ◽  
F. Balloux
2013 ◽  
Vol 49 (2) ◽  
pp. 279-288
Author(s):  
A. A. M. Elhassan ◽  
A. A. Hussein ◽  
H. S. Mohamed ◽  
K. Rockett ◽  
D. Kwiatkowski ◽  
...  

2005 ◽  
Vol 202 (2) ◽  
pp. 197-201 ◽  
Author(s):  
Jean-Laurent Casanova ◽  
Laurent Abel

The immune system's function is to protect against microorganisms, but infection is nonetheless the most frequent cause of death in human history. Until the last century, life expectancy was only ∼25 years. Recent increases in human life span primarily reflect the development of hygiene, vaccines, and anti-infectious drugs, rather than the adjustment of our immune system to coevolving microbes by natural selection. We argue here that most individuals retain a natural vulnerability to infectious diseases, reflecting a great diversity of inborn errors of immunity.


2013 ◽  
Vol 49 (2) ◽  
pp. 246-254
Author(s):  
A. A. M. Elhassan ◽  
A. A. Hussein ◽  
H. S. Mohamed ◽  
K. Rockett ◽  
D. Kwiatkowski ◽  
...  

2003 ◽  
Vol 25 (6) ◽  
pp. 15-18 ◽  
Author(s):  
Andrew Prentice ◽  
Conor Doherty ◽  
Joann McDermid ◽  
Sarah Atkinson ◽  
Sharon Cox

Young children in rural Gambia face constant exposure to gastrointestinal and respiratory infections and, during the rainy season (July–November), suffer recurrent bouts of Plasmodium falciparum malaria. Within living memory, these conditions led to more than half of the children dying before their fifth birthday, providing a graphic demonstration of the impact that infectious diseases have had on our natural selection. Fortunately, these horrific statistics have been decreased greatly by improved medical care, especially through vaccination and anti-malarial therapies, but conditions such as these have inevitably left a powerful imprint on man's genetic make-up.


2020 ◽  
Author(s):  
David V. McLeod ◽  
Geoff Wild ◽  
Francisco Úbeda

AbstractGenes with identical DNA sequences may show differential expression because of epigenetic marks. These marks in pathogens are key to their virulence and are being evaluated as targets for medical treatment. Where epigenetic marks were created in response to past conditions (epigenetically inherited), they represent a form of memory, the impact of which has not been considered in the evolution of infectious diseases. We fill this gap by exploring the evolution of virulence in pathogens that inherit epigenetic information on the sex of their previous host. We show that memories of past hosts can also provide clues about the sex of present and future hosts when women and men differ in their immunity to infection and/or their interactions with the sexes. These biological and social differences between the sexes are pervasive in humans. We show that natural selection can favour the evolution of greater virulence in infections originating from one sex. Furthermore, natural selection can favour the evolution of greater virulence in infections across sexes (or within sexes). Our results explain certain patterns of virulence in diseases like measles, chickenpox and polio that have puzzled medical researchers for decades. In particular, they address why girls infected by boys (or boys infected by girls) are more likely to die from the infection than girls infected by girls (or boys infected by boys). We propose epigenetic therapies to treat infections by tampering with the memories of infecting pathogens. Counterintuitively, we predict that successful therapies should target pathogen’s genes that inhibit virulence, rather than those enhancing virulence. Our findings imply that pathogens can carry memories of past environments other than sex (e.g. those related to socioeconomic status) that may condition their virulence and could signify an important new direction in personalised medicine.


PLoS ONE ◽  
2021 ◽  
Vol 16 (2) ◽  
pp. e0246278
Author(s):  
Daniele Vilone ◽  
John Realpe-Gómez ◽  
Giulia Andrighetto

Cooperation is crucial to overcome some of the most pressing social challenges of our times, such as the spreading of infectious diseases, corruption and environmental conservation. Yet, how cooperation emerges and persists is still a puzzle for social scientists. Since human cooperation is individually costly, cooperative attitudes should have been eliminated by natural selection in favour of selfishness. Yet, cooperation is common in human societies, so there must be some features which make it evolutionarily advantageous. Using a cognitive inspired model of human cooperation, recent work Realpe-Gómez (2018) has reported signatures of criticality in human cooperative groups. Theoretical evidence suggests that being poised at a critical point provides evolutionary advantages to groups by enhancing responsiveness of these systems to external attacks. After showing that signatures of criticality can be detected in human cooperative groups composed by Moody Conditional Cooperators, in this work we show that being poised close to a turning point enhances the fitness and make individuals more resistant to invasions by free riders.


Author(s):  
Sylvia Abonyi

In a 1949 landmark paper Haldane proposed that infectious diseases may act as agents of natural selection. Apart from the well-established link between sickle-cell anaemia and malaria, direct evidence for the selective effect of infectious disease is scarce. There is some evidence to suggest that blood group O individuals may be more susceptible than individuals from other blood groups to life-threatening cholera infections. Cholera is endemic to the Ganges River Delta in India, a region whose current population appears to represent the lowest global frequency of the 0 allele. Using a model proposed by Svanborg-Eden and Levin (1991) as the framework of investigation, this paper evaluates the evidence for cholera operating as an agent of natural selection in the Ganges River Delta. This model proposes a series of six conditions that must be met in order to accept an infectious disease-mediated selective effect. All six conditions could not be satisfied by the existing evidence, and it is therefore concluded that cholera cannot be accepted as further evidence of infectious diseases acting as agents of natural selection in human populations.


Parasitology ◽  
1992 ◽  
Vol 105 (S1) ◽  
pp. S103-S105 ◽  
Author(s):  
M. J. Doenhoff ◽  
A. J. S. Davies

SUMMARYEvidence has accrued to indicate that host defence mechanisms enhance the efficacy of many of the drugs used to treat infectious diseases. Because of this, and also because of the likelihood of increased pathogen loads in immunoincompetent hosts, some infections are less likely to be completely cured by normal regimens of chemotherapy in individuals with drastically impaired immune responsiveness. In such circumstances natural selection could result in the accelerated emergence of drug-resistant pathogens.


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