Creationists who claim that biologists are abandoning the Theory of Evolution in favour of intelligent design might benefit from looking at what biologists actually do, if only they could find the courage to read some actual science.
A good place to start would be the research of Howard Hughes Medical Institute investigator Harmit Malik and his colleagues, who investigate how genetic conflicts drive evolutionary change. Here, evolution is a working scientific framework: it supplies questions, generates testable predictions and helps researchers explain their experimental results.
No supernatural designer is required.
A study led by Tamanash Bhattacharya and published in Science Advances describes this research programme. Working with Sindbis virus, the researchers investigated how an unusual genetic stop signal helps the virus evade its hosts’ immune defences.
This signal, known as the opal stop codon, helps maintain the integrity of tiny compartments in which the virus copies its RNA, shielding that RNA from immune detection. Its importance therefore depends on the opposition the virus encounters. In mosquito cells with functioning antiviral defences, selection strongly favoured viruses carrying the stop signal. Within five days — approximately 24 rounds of replication — viruses that had regained it almost completely replaced a variant lacking it. When the relevant host defence was disabled, the selective advantage changed, and variants without the stop signal could prevail.
That is evolution measured in the laboratory: heritable variation, differential reproductive success and a resulting change in the genetic composition of a population. The experiment reveals a mechanism through which host immunity shapes viral evolution. It also illustrates why “fitness” has no meaning independently of circumstances. A genetic variant advantageous in one environment can become disadvantageous when that environment changes.
Such conflicts make straightforward sense in evolutionary terms. Hosts benefit from restricting infection, while viruses benefit from overcoming those restrictions. Over evolutionary time, adaptations on either side can impose selection for counter-adaptations on the other. There is no foresight, agreed destination or concern for the welfare of the opposing side — simply competing lineages leaving different numbers of descendants.
For the notion of a single, omniscient, benevolent designer, however, this raises an awkward question. Why devise an immune system to detect and suppress a virus, then equip the virus with a mechanism for concealing itself from that same immune system? What coherent protective purpose is served by supplying both the defence and the means of defeating it? Invoking an inscrutable intention can accommodate any outcome, but it explains none of the experimental detail and supplies no competing prediction.
As I discuss in my books, The Unintelligent Designer: Refuting the Intelligent Design Hoax and Unintelligently Designed Arms Races: How Nature Refutes Intelligent Design, these recurrent conflicts are precisely what we should expect from evolution without an overarching plan. Attributing them to one designer instead makes that designer responsible for undermining its own supposed protective arrangements. Treating today's solutions as problems to be overcome with fresh solutions tomorrow, ad infinitum, is the antithesis of intelligent design, but the predictable outcome of blind evolution.
Meanwhile, scientists continue to use evolutionary theory to discover how these systems work. This research provides a concrete example of that theory’s continuing productivity, whatever creationist publicity might claim.
Evolutionary Arms Races^ Why Neither Side Wins for Good. An evolutionary arms race develops when an adaptation in one lineage creates selection pressure for a counter-adaptation in another. Hosts evolve defences against infection; pathogens evolve ways of evading or overcoming those defences. Each can change the conditions under which the other must survive and reproduce.The study published open access in Science Advances was announced in a news release from the Howard Hughes Medical Institute:
The military terminology is a metaphor. Neither side plans its next move, recognises a problem or deliberately invents a solution. Mutations and other sources of genetic variation arise without regard to what an organism needs. Natural selection then favours heritable variants that leave more descendants under the prevailing conditions.
How the cycle works
- Variation already exists or arises: some hosts resist infection more effectively than others, while some pathogen variants are better at infecting particular hosts.
- Selection changes the population: if resistance improves survival and reproduction, the responsible host variants can become more common.
- The selective environment changes: pathogens now encounter more resistant hosts, favouring variants capable of overcoming that resistance.
- Counter-adaptation becomes advantageous: successful pathogen variants can, in turn, favour further changes in host defences.
This reciprocal evolutionary change is called coevolution. However, demonstrating that a pathogen adapts to a host defence is not, by itself, evidence that both sides evolved during the same experiment. Establishing reciprocal change requires evidence from both lineages.
The Red Queen: Running to Stay in the Same Place
The Red Queen hypothesis takes its name from Lewis Carroll’s Through the Looking-Glass, in which running can be necessary merely to remain in the same place. In evolutionary biology, the analogy describes how a lineage may need to keep evolving to maintain its relative success because the organisms with which it interacts are also evolving.
A defence that worked well against yesterday’s pathogens may work less well against their descendants. Likewise, a pathogen’s successful means of entry may become less effective as resistant host variants spread. Evolution has no final, universally optimal solution because the conditions favouring any particular solution can change.
Nor must every arms race produce ever greater complexity or an endless escalation. Adaptations can carry costs, resistance can remain incomplete, and different variants can rise and fall in frequency. Sometimes losing or reducing a feature is advantageous. Extinction, changes in host use and ecological shifts can also alter or end a particular contest.
Fitness Depends on the Opposition
In evolutionary biology, fitness means reproductive success relative to other variants in a particular environment. It does not mean strength, sophistication or perfection.
A viral feature that helps conceal its RNA from a host’s immune machinery may be advantageous when that machinery is functioning. If the relevant defence is absent, the benefit can disappear, and a different variant may reproduce more successfully. The host’s defences are therefore part of the virus’s selective environment.
Different Evolutionary Timescales
Viruses can pass through many replication cycles within a single host generation. Large populations and rapid replication can give selection repeated opportunities to favour advantageous variants. Hosts, however, are not starting from scratch: their populations already contain inherited variation, and they possess multiple layers of defence.
It is also important to distinguish an immune response within an individual from evolution across host generations. Switching on antiviral genes during an infection does not mean that the host population has evolved. Population-level evolution involves changes in inherited characteristics across generations.
What the Sindbis Virus Study Shows
The researchers demonstrated rapid viral evolution under selection imposed by host immunity. Different viral variants prospered depending on whether a particular antiviral defence was functioning. This reveals one part of the machinery of an evolutionary arms race; it does not mean that the mosquitoes and viruses completed a reciprocal cycle of coevolution during the experiment.
Brief Glossary
- Selection pressure
- An environmental influence that causes heritable variants to differ in survival or reproductive success.
- Fitness
- Relative reproductive success in a particular environment.
- Adaptation
- A heritable feature shaped by natural selection because it improves reproductive success under particular conditions; also the process producing such features.
- Coevolution
- Reciprocal evolutionary change in interacting lineages, each imposing selection on the other.
Surveying the Genetic Battlefield to Uncover the Rules of Rapid Evolution
HHMI Investigator Harmit Malik and his team are studying how viruses and proteins rapidly evolve to keep up with their foes, providing insights that could inform the development of new antivirals.
KEY TAKEAWAYSThe Malik Lab thrives on competition. But for HHMI Investigator Harmit Malik and his team at the Fred Hutchinson Cancer Center, it’s the genomes — not the people — that are in conflict.
- HHMI Investigator Harmit Malik and his team study genetic conflicts, like virus-host competitions, to understand how different players rapidly evolve to maximize their own success.
- In new research, the team discovered how alphaviruses have evolved a strategy to successfully infect both mosquitoes and humans. Uncovering the strategies molecular rivals employ in these conflicts could help researchers develop new ways to combat diseases, including new antiviral medications.
The lab studies rapid evolution — the genetic changes that happen in a species over a few generations rather than thousands of years. These fast changes are often fueled by genetic conflicts — competitions between different entities trying to maximize their success at the expense of another.
By uncovering the evolutionary rules that guide these conflicts, Malik and his team are revealing insights that could help in the development of better disease treatments.
Not only do these rules help us to look back in evolution and understand how these arms races played out, but these rules also let us look forward and come up with new strategies.
Harmit S. Malik, co author
Basic Sciences Division
Fred Hutchinson Cancer Center
Seattle, WA, USA.
Discovering a Viral Thermometer
One of the competitions the lab studies is the conflict between mosquito-borne alphaviruses like Sindbis and Chikungunya and their hosts. These viruses are successful at infecting both insects and humans despite the different body temperatures and immune systems of these hosts. The team, including postdoc Tamanash Bhattacharya, recently uncovered a carefully calibrated system that helps enable this versatility. A special stop codon in the virus’s genome, which signals the cell to halt protein production, enables a “kinetic goldilocks”: It allows the virus to produce just enough of a critical polyprotein to survive, but not too much to slow down other processes that would lead to a decline in the virus’s fitness.
In humans, where body temperatures are hotter and replication happens quickly, the virus relies on this codon, called the opal codon, to enable this production balancing act. In mosquitoes, where temperatures are colder and replication slows down, this balancing act isn’t necessary, and the virus does not need to rely on this special stop codon.
HHMI Investigator Harmit Malik (center) with Jeremy Hollis (left) and Tamanash Bhattacharya (right) are working to understand how viruses and proteins rapidly evolve.Credit: Aida de la Cruz.
Hiding from the Immune System
These insights led the team to another question: Why is the opal codon still found in alphaviruses that only infect mosquitoes, even though its special properties aren’t needed? In new research, also led by Bhattacharya, the team found that in both humans and insects, the opal codon enables the virus to create a compartment where it can replicate without being seen by the host’s immune system. If the opal codon is lost, viral replication becomes more visible and more susceptible to host immunity.This is one of the simplest and most elegant ways to hide yourself from immunity, and the fact that it is universally conserved in alphaviruses just reinforces how important it is.
Harmit S. Malik.
Now, the team is working to understand other built-in strategies these viruses use to thrive in different hosts, including the ability to quickly ramp up fitness in one host at the expense of the other.Learning the rules by which they do this gives us insight into the sheer adaptive possibilities that these genomes can experience. That’s important because any attempts to make new antivirals will have to take this into account.”.
Harmit S. Malik.
Evolution of Essential Genes
It might seem counterintuitive, but essential genes that organisms need to survive, grow, and reproduce are often among the fastest evolving. The Malik Lab is uncovering these changes and why they occur.
- New research, led by graduate student Jeremy Hollis, examines HJURP, a chaperone protein that marks the centromere, the site where chromosomes are pulled apart during cell division. Despite its importance, scientists couldn’t find HJURP in many animals. The Malik Lab used remote homology detection, AlphaFold-based structural modeling, and functional genetic techniques to show that most animals do have HJURP. Because the protein evolves so rapidly, possibly to keep pace with other fast-changing centromere components, conventional tools couldn’t detect it.
- Separate research, led by former postdoc Ching-Ho Chang, investigated Mst77F, a protamine that packages DNA in fruit fly sperm. Protamines, which are essential for male fertility, are among the fastest-evolving genes in animals, and scientists couldn’t figure out why. The Malik Lab found that Mst77F is rapidly evolving to suppress a form of genetic cheating that kills X-bearing sperm and skews broods toward sons.
Publication:
Far from showing biologists abandoning the Theory of Evolution, this research shows them using it to ask productive questions and obtain experimentally testable answers. Why is a particular genetic feature retained? Under what conditions does it confer an advantage? What happens when the selective pressure changes? These are evolutionary questions, and the results make sense in terms of mutation, inheritance and differential reproductive success. Intelligent design contributes no additional explanatory mechanism.
The speed of the observed changes also exposes the familiar misconception that evolution is necessarily too slow to observe. Here, substantial changes in the genetic composition of viral populations occurred within days. The researchers did not merely identify a useful viral feature and invent a plausible story about it: they investigated how its advantage depended on the host’s antiviral defences. Evolution was something they could measure, and the selective environment helped explain its direction.
For intelligent design creationism, the deeper difficulty is the conflict itself. The same putative designer must receive credit for the host’s protective machinery and for the viral mechanism that helps evade it. Praising the ingenuity of one while ignoring the other simply conceals the contradiction. As I discuss in The Unintelligent Designer and Unintelligently Designed Arms Races: How Nature Refutes Intelligent Design, attributing both sides to a single, omniscient, benevolent agency turns biological defence into an exercise in deliberate self-sabotage.
Evolution requires no such contortions. What benefits the virus need not benefit its host, and natural selection has no responsibility to reconcile their competing interests. There is no shared plan and no foresight — only heritable differences whose consequences depend on the circumstances. Once again, scientists investigating how nature works have produced findings that are readily intelligible within evolutionary biology, while leaving creationists to explain why their supposedly intelligent designer keeps undermining its own work.
Advertisement
Amazon
Amazon
Amazon
Amazon
Amazon
Amazon
Amazon
Amazon
Amazon
Amazon
Amazon
Amazon
All titles available in paperback, hardcover, ebook for Kindle and audio format.
Prices correct at time of publication. for current prices.
No comments :
Post a Comment
Obscene, threatening or obnoxious messages, preaching, abuse and spam will be removed, as will anything by known Internet trolls and stalkers, by known sock-puppet accounts and anything not connected with the post,
A claim made without evidence can be dismissed without evidence. Remember: your opinion is not an established fact unless corroborated.