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Tuesday, June 18, 2024

An Ode to Parasites: How infections made us who we are today…

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Haseeb Irshad
Haseeb Irshadhttps://scientiamag.org/
Haseeb Irshad is a neophyte connoisseur of academic writing, whose interests range from medicine, bio-molecularity, and environmental and ecological studies to pop-culture TV and films. He also indulges in fiction and religious studies from time to time.

Let’s get this straight right away: Bacteria and viruses, specifically the infectious and harmful type have practically propelled us through millennia, molding our genomes into their current state, allowing us to become the apex species that we now are. In a nutshell, we owe our uniqueness, our sexual mode of reproduction and even an arguably premature death to these foes.

You might be wondering, what has prompted the author to accredit the despised, disease-causing, sickness-inducing microbes with such a monumental achievement. What, you may think, could be the role of these little troublemakers, when the entire body, day in and night out is pouring out an endless stream of defense mechanisms against them? At the first glance, it doesn’t make sense that organisms that our body fights tooth and nail to keep out, could be the very architects of our genome.

But here’s the plot-twist in the saga: the pathogens have never intended anything beneficial for us, indeed they’ve been trying their very best to bring us down. But this has backfired for them every single time. Let’s travel back to the very beginning of life.

How it started?

Nearly 700 million years ago, our first multicellular grandparents crawled out of the murky waters of Earth. However, upon emerging they found their surroundings wholly infested with single-celled and even colonizing micro-organisms. Those micro-organisms had spent the last 3 billion years competing for resources and niches (habitats) to fill.

It did not take them long to infiltrate the tissue of the multicellular newbies. They walked into the bodies of the multicellular organisms and began making adjustments to their new home. They poked and prodded, ate from the tissue and secreted toxins. In essence, they became parasitic and caused sickness.

All this in the name of selfishly adapting to their new hosts. This is where a bit of Darwinian Magic or Divine Will allowed mutations in the genomes of the multicellular organisms. The same mutating force, which had led them to the threshold of multicellularity, was not about to abandon them at this stage. The events of genetic variations between successive generations ultimately allowed some (or one) of the mutants to adapt to the parasitic problem of the microbes and survive the first onslaught.

The wheel gets rolling

As the multicellular organisms saw the first amendment/addition of resistance to their genome in the aftermath of their first battle with the microbes, the tone for the majority of evolution was set. From there on, our multicellular grandparents fought countless such wars with the microbes, and similar to sustaining post-war scars, they collected genome sequences or “genes” resistant to a myriad of diseases.

Their genomes grew in size, complexity, and sophistication. So much so that millions of years later, we have an enormous genetic corpus of additions from each of those encounters. For instance, our pathogen-recognition genes or HLA (Human Leukocyte Antigen) have no less than 12,000 variants1.

To put that in perspective, that is almost a hundred times more varied than any other part of our genome. This is an anomaly in stark contrast with the rule of thumb for evolution, which tends to simplify the genome of any unnecessary and burdensome variations. To say that 12,000 is a cumbersome quantity of variations to retain is an understatement.

Multicellular organisms
Our pathogen-recognition genes or HLA (Human Leukocyte Antigen) have no less than 12,000 variants

According to the modern understanding of our genetic pedigree, the only reason we have not gotten rid of most of these variants, many of which correspond to resistance against ancient and long-forgotten diseases, is that each microbe associated with the variants keeps returning, stronger each time, having evolved in the span of days or even hours. It’s like we keep a specialized diary of each version of each infectious microbe, that is handed down the generations, and is updated with each new encounter. The shocking part is that some of the genes we carry around today are 30 million years old2.

Is a “Thank You” in order?

Even more astoundingly, these pathogens caused the refinement of the human race. According to the University of California Bio-molecularity expert, Ajit Varki, 2 million years ago, a malaria-like pathogen attacked the hominid tribe (made up of Australopithecus, Homo habilis, – erectus, and sapiens). It targeted all organisms which produced certain Sialic acids3.

It manipulated the acids to gain access to the interior of the host cells, wherein it fulfilled its parasitic tendencies, causing the cell and then the host to collapse. In simple terms, due to its potent virulence and lethal effects, it caused the eventual extinction of all the members of the hominid tribe except a few deficient in sialic acid production. These few would go on to become the forefathers of Homo sapiens or modern humans.

Enter, Sexual reproduction!

It was to avoid such disasters of complete extinction on the part of host species that only after one billion years of exposure to pathogenic aggression, sexual reproduction was taken up by them; simply to create as many genetically unique variants of themselves in hopes of avoiding death at the hands of a single-minded pathogen. Before, these organisms had to rely completely on genetic mutations between asexually produced generations. However, as the word “mutation” suggests, there wasn’t much thought going into the process. More often than not, the mutations would produce variations that worsened the genome, downright reducing the organism’s chances of survival.

As a counterpoise, sexual reproduction evolved which allowed the organisms to make sober decisions about mixing their genome with another superior and preferred genome. Even today, if a woman inexplicably finds herself attracted to the broad chins or deep-set eyes, or even the body odor4 of a potential mate, it is entirely thanks to the internal biological mechanism picking up hormonal or pheromonal signs of health and virility, since austere facial features signal high testosterone levels while contrasting body odor is a sign that their offspring will be immunologically well-endowed.

All shall taste death

Looking closely at the inner structure of the DNA, we are surprised to find “Suicide Genes” that are responsible for automatically turning off the cell machinery at a certain time frame. To a rational mind, the fact that our body refuses immortality when it is entirely within reach, is strange to say the least. Why our cells simply stop dividing at a certain age is one of the greatest secrets of human biology.

Indeed, organisms around us like trees, have not opted out of the possibility of immortality. They continue to live as long as they are sheltered from physical and chemical trauma, and certainly only grow stronger as they age. Why we become weaker with each passing year while trees grow mightier is also answered by the role of pathogens in our long history with them.

Looking closely at the inner structure of the DNA, we are surprised to find “Suicide Genes” that are responsible for automatically turning off the cell machinery at a certain time frame.
Looking closely at the inner structure of the DNA, we are surprised to find “Suicide Genes” that are responsible for automatically turning off the cell machinery at a certain time frame.

The drawback of being an immortal species, as Sonia Shah puts it, is quickly expanding to occupy its limits in an ecosystem. Under normal circumstances, such an outcome is quite favorable, but in the chance of a natural disaster or more appropriately a “pandemic” from parasitic microbes means that the entire species stands at a risk of being wiped off the face of Earth. Similar to how a sparsely spaced forest has a greater chance of surviving a fire than a thick and dense one.

The Red Queen

This theory of evolution of sex and suicide genes5, is jointly called as the “Red Queen Hypothesis6, a grim reference to Lewis Carroll’s Alice in Wonderland, where despite running for a while, Alice can’t seem to move away from where she is. To this, the Red Queen of Hearts tells Alice she must run twice as fast to get anywhere!

Similarly, the relationship between pathogens and hosts is one of a constant cycle of adaptation, evolution and resistance, with both parties having ran significantly at the end of the day, with no real change in the balance of power. If the pathogen mutates to become more viral or infectious, after some initial success, it begins to falter as the host adapts and becomes resistant to its mechanisms.

It is the consequences of this cat-and-mouse strategy of evolution that our bodies spend enormous amounts of energy patrolling our tissue against pathogens, with thousands of white blood cells, extremely acidic and basic mediums and layered membranes. Essentially, making us who we are as organisms, in regards of genetic complexity, sophistication of defenses and a general psychological bias against anything remotely sickness-inducing.

Outlook

Even today, as surgeons rush to transplant organs and suppress the immune reactions of host patients, as women subconsciously pair with men that boast opposite immune system configurations from their own, and as new pathogens jump the boundary from the wild into humans in novel cases of zoonosis, the genomic grounds are seeing imperceptible but tectonic shifts in their layout. As new genes of resistance and immunity are being added and the arsenal of protective measures grows, so does the human race evolve into its next era.

References

  • 1,2 Shah, Sonia. “Pandemic: tracking contagions, from cholera to Ebola and beyond
  • 3 Ajit Varki, “Human Specific Changes in Siglec Genes”
  • 4 Meyer and Thomson, “How selection shapes variation of the human major histocompatibility complex”
  • 5 Mitteldorf, Josh; Pepper, John. “Senescence as an adaptation to limit the spread of disease
  • 6 Hamilton, William. “Sexual reproduction as an adaptation to resist parasites

Also Read: ROLE OF GENETICS IN INFECTIOUS DISEASES SPREAD, GENETICAL EVOLUTION

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