Co-evolution is a situation where two or more species influence each other’s evolution reciprocally by applying selective pressures on each other. Genetically speaking, co-evolution is the change in genetic composition of one species in response to the genetic change in another. This can lead to evolutionary ‘arms races’, a classic example being the interaction between plants and insects. The development of a gene for chemical defences that is harmful to the insect by the plant will put a pressure on the population growth of the insect, and the insect will try to overcome this by evolving something to detoxify them, the plant will in turn evolve a stronger defence and so on, without either side ‘winning’ (Ridley 2004). There are different types of interactions between organisms (Maynard Smith 1998). Among some are:
Competition, where 2 species compete for a limited amount of a common essential resource and one or the other will be eliminated. For example, lions and cheetahs both feed on similar prey, so they are negatively affected by each other because they will have to compete for food.
Mutualism, where the presence of one species stimulates the growth of another, and both sides benefit from the relationship, such as animals like cow and bacteria within their intestines. Cows benefit from cellulase produced by bacteria to help digestion while bacteria benefit from having nutrients supply from the cows.
Parasitism, host-pathogen co-evolution, interaction between humans and disease organisms is an example of this, where a parasite benefit from its host at the cost of the host.
In the mid-nineteenth century, Charles Darwin and Alfred Russel Wallace determined the mechanism of evolution as natural selection. Species and population do not remain fixed, but they change over time. Individuals of a same species show differences in phenotype, such as difference in height, colour, or defences against enemies. These can be passed on through generations. In a community, members of the same species will need to struggle for limited resources and avoid predators for survival. Those with an advantage in phenotype will survive better and therefore be able to reproduce more successfully. One way to recognize natural selection in a population is by using the Hardy-Weinberg equilibrium to measure the allele frequencies and genotype frequencies, on the assumption that it is an ideal population with large population size and random mating, lack of mutation and migration. There are three main types of selection:
Directional selection, where the phenotype at one end of the distribution is selected for and the other end selected against.
Stabilizing selection, where the intermediate phenotype is selected for while those at both extremes are selected against.
Disruptive selection, where the phenotypes at both extremes are favoured simultaneously.
In addition to natural selection, other factors that could alter allele frequencies are like mutation, migration or genetic drift that might eventually lead to speciation, which is the formation of new species (Klug, Spencer et al. 2007).
Disease organisms are called pathogens, causing diseases by infecting or infesting another organism. They are often described as parasite, because they benefit from living in or on a host, at the cost of the host and can be anything from microorganisms such as bacteria and viruses to parasitic worms like tapeworms. To discuss the interaction between humans and disease organisms, we first have to look at how humans protect themselves against infection. The first line of defence of humans against pathogens is physical barriers. The intact skin of humans serves as an impenetrable barrier to pathogens and the acidity of sweat also hinders growth of bacteria. However, pathogens can still get inside the human body and this is where the immune system comes into play. There are two mechanisms of the immune system, namely the innate immunity and the adaptive immunity. Innate immunity is the inborn ability to defend ourselves without prior learning experience and this includes phagocytes such as monocytes and neutrophils where they can ‘eat’ up the pathogens, and inflammatory cells such as eosinophils and basophils that trigger local inflammation at the infection site. On the other hand, adaptive immunity is the immune response that needs to be acquired through experience and it has exquisite specificity and immunological memory. The cells working under adaptive immunity are like cytotoxic cells that kill infected cells and B cells that produce antibody to destroy pathogens. On the timeline of evolution, humans, or Homo sapiens have only been around for less than 2 million years, while worms have been around for about 750 million years. The complexity of the innate immunity in humans today is due to evolution as time passes and more species of pathogens appeared, because only the fittest individuals survived the infection to reproduce and pass on their genes to the next generation. Innate immunity provide immediate defence against infection but it only recognises prominent differences between own cells and the pathogens, therefore responding to pathogens in a generic way. Thus, innate immunity works closely together with adaptive immunity which can give long term specific immune response due to memory cells. For example, immunity for malarial parasite will not give immunity for bacteria that causes tuberculosis (Davey, Halliday et al. 2001). Exposure to a certain pathogen in varying degrees also has affect on the genetic evolution of the immune system. One example is a cluster of genes that plays an important role in the recognition and presentation of non-self antigens to the cells of the immune system called the HLA (human leucocyte antigen), also known as major histocompatability complex (MHC) has been found to have associations with diseases like leprosy and tubercolosis (May and Anderson 1983). In a human population exposed to more of the diseases shows a higher diversity on the HLA genes.
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Disease organisms have different generation times. For example, the bacterium Escherichia Coli can reproduce in just twenty minutes under ideal circumstances, while the HIV (Human Immunodificiency Virus) can generate 10 billion new virus particles in a day. So in the course of the human’s life, these pathogens can go through hundreds and thousands of generation, evolving to become better adapted and acquiring counter-defence to the human’s immune system. Some important features of the co-evolution of humans and disease organism arise from this huge difference of reproductive rates. Pathogens usually possess certain adaptations to resist humans from trying to remove them and they are very much dependant on humans as their hosts for essential resources to survive, grow and reproduce. They must be able to find a new host before their current one dies or make their transition by means of vector species. The activity of the pathogens will to some extend reduce the fitness of humans or even kill them. There is a varying degree of harm that a pathogen can cause to humans, and this property is called virulence. For the same species of pathogen, some individuals might be totally unaffected by it while some might get infection that could be mild to serious or even killed by it. Virulence of one pathogen can be measured as the percentage of infections that leads to death. The bacterium Vibrio cholera was one the most virulent human pathogens, with a virulence of 15 percent until the appearance of HIV, which has a virulence of over 90 percent, meaning that 90 percent of infected people die (Davey, Halliday et al. 2001).
There are different phases in which a disease organism can adapt to its host. The first phase being accidental infection, that is the first contact of the pathogen with a new species of host. Many human diseases are caused by pathogens that infect animals such as rabies, SARS and bird flu. Host changes are promoted by frequent contact between humans and animals such as keeping a pet. The second phase is the evolution of virulence after the pathogen has successfully invaded a new host. In this phase evolution of virulence happens rapidly because the pathogen is not be well adapted to the new host and will try to overcome the immune response by the host. The third phase occurs the pathogen has been persisting in the new host for some time and tries to reach an optimal virulence. Virulence that is too high either kills the host too quickly resulting in less time to reproduce successfully , reduce the chances of the host interacting with other hosts therefore reducing transmission or induces an immune response that react too strongly, while mildly virulent strains will be cleared by the immune system too quickly (Stearns and Koella 2008). An example of co-evolution between the immune system of humans and disease organism is shown in flu virus. When a large proportion of the population has developed immunity to a certain strain of flu virus, the spread of the virus will be prevented until it has evolved by mutation or re-assortment. This is called antigenic drift, where a variety of strains are created until one can infect people who are immune to the pre-existing strains. If a virus is produced that has entirely new antigens, everyone will be susceptible thus causing a major pandemic.
Possibly one of the best-known cases for co-evolution of humans and disease organisms is the evolution of humans for the sickle cell trait to protect against severe malaria. Sickle cell disease is caused by a change in shape of haemoglobin, causing red blood cells to be distorted and encounter problems when passing through blood capillaries. Homozygous individuals do not survive for long and rarely reproduce while heterozygous individuals produce sickle shaped red cells and normal ones but barely develop any symptoms of the disease. One would assume that the allele frequency of sickle cell would reduce in a population but this is not the case. It has been found that heterozygotes for sickle cell have an advantage over normal individuals because the sickle shaped red cells reduce the ability of the parasite Plasmodium to grow and multiply. Another example that can be given is the evolution of the bacterium such as Mycobacterium tubercolosis, which causes TB. Strains of the TB bacterium have evolved recently that is resistant to all drugs, namely the multi-drug resistant (MDR) strains. Depending on the changes in human population, the bacteria can change its virulence accordingly. Some pathogens are willing to trade-off virulence with transmission, keeping virulence low so that transmission between hosts can happen. However, if the host becomes abundant or the immune system is suppressed as in the case of AIDS, then the pathogen may evolve a higher virulence.
Co-evolution simply means the evolution of one species in response to that of another species. However, co-evolution does not indicate dependence on one another. Humans are not dependant on parasites for survival, and the other way around. Co-evolution of humans and disease organisms has produced many fascinating variations, whether in humans or the disease organisms. The studies on this can aide us in gaining understanding of health and diseases as disease organisms remain a major cause of mortality, especially in the under-developed regions of the world.
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