Healing Psychology, Part F - Viral Origins.

In the last episode of this series, we described self-repeating, malignant behaviors – habits such as alcoholism and anorexia nervosa – as true diseases. In fact, these patterns of behavior have many of the features of viruses. Like viruses, they are simple patterns – so simple that they can get themselves repeated only by exploiting the capabilities of their hosts. They begin as normal habits, but they escape our control. They end up acting like parasites, with us as their hosts. 

Today’s psychology doesn’t support the idea of parasitic habits. But it should. Psychology is a part of biology, its mother science. In biology, parasitism is everywhere you look. It would be wise, then, to expect parasitic forms in our behavior. As we struggle to understand how a habit could turn parasitic, we should consider the origin of biological viruses. Because virus-like habits come about in pretty much the same way. 

Transcript

Part F - Viral origins
This episode of Healing Psychology is a reading of Chapter Five of my upcoming book, Reimagining Psychology.
Copyright (c) Thomas O. Whitehead, 2022. All rights reserved

[Introduction]

Welcome to Part F of the multi-part series “Healing Psychology.” In previous episodes, we’ve interpreted addiction and anorexia as habits that have escaped the individual’s control, and have become true diseases. We’ve stressed that these rogue habits have many of the features of viruses. Like viruses, they are simple patterns that can get themselves repeated only by exploiting the capabilities of their hosts. Though they begin as normal habits, these wayward behaviors manage to dodge our usual methods of control. They end up as parasites, repeating themselves over and over, with us as their unwilling hosts.

Psychology is a part of biology, its mother science. In biology, parasites are everywhere you look. So, we shouldn’t be surprised to find parasitic forms in our behavior, once we know what to look for. As we struggle to understand how a habit could turn parasitic, it helps to know how biological viruses come into being. Because virus-like habits arise in pretty much the same way.

Today’s psychology doesn’t support the idea of parasitic habits. But you’re invited to listen … anyway.

[Reading]

• The escape or vagrancy (cell-first) hypothesis  describes viruses as derived from cellular RNA or/and DNA  fragments… which escaped from cells. When such RNA or DNA  fragments acquired protein coat they became independent  entities capable of infecting cells from which   they had escaped previously. [1]

- Julia Durzyńska and Anna Goździcka-Józefiak 

We can’t doubt that viruses are real. Every one of us has had to cope with the illnesses they cause. But not everyone has wondered where they come from. Do we really need to know? Someone steeped in our current psychology may not see any reason at all to be curious about viral origins. But there is a connection.

Psychology is a part of biology. Understanding how viruses originate in our biology can help us understand how strange, virus-like patterns—self-sustaining patterns like alcoholism and anorexia—can develop in our behavior. Surprisingly, as we come to understand this, we begin to understand how conscious awareness fits into the picture. 

There are, of course, big differences between the self-reproducing strings of chemicals we call viruses, and self-reproducing, virus-like strings of behavior. In the virion stage of their life cycle, biological viruses have physical forms, things we can even photograph. In that stage they are particles, tangible objects, tiny nuggets of chemicals that are seemingly lifeless on their own. They blossom into something alive only when unleashed within their host cells. 

How should we think of a cell’s behavior, before and after viral infection? The activity of a cell is the interaction of chemical molecules. The life cycle of a biological virus involves swinging back and forth between its existence as a physical object outside the cell, and its existence as a chemical-behavioral process within its host cell. 

Behavioral viruses—virus-like habits—are different. They don’t take on a physical form at any stage of their reproduction. They are 100% behavior—all behavior, all the time. [2] At no point during their self-repeating cycle do they gain a tangible form of their own. [3] There’s nothing you can see, nothing you can touch or photograph. That makes it harder to believe they’re real.

And there’s a big difference in the speed of their evolution. Where biological viruses evolve slowly, over many, many generations, behavioral viruses can arise in practically the blink of an eye, within one single individual. Nevertheless, both biological and behavioral viruses come into being through a similar mechanism, and for similar reasons. That’s why understanding one can shine light on the other.

An origin story

Let’s take a closer look at biological viruses. As I have stressed, they contain much, much less genetic information than their host cells. Remember that they don’t need a lot, because they exploit their hosts’ genetic information. Despite their simplicity, viruses have what it takes to reproduce themselves, as long as they can exploit the greater capabilities of their more complex hosts. 

Viruses are so simple that virologists don’t consider them full-fledged living organisms. Yet no authority doubts that they can reproduce, and no one doubts that they evolve. Though they may not be alive in themselves, it doesn’t hurt to think of viruses as “lifeforms.” After all, their merging with a living host creates something that’s undeniably alive. 

For decades, the question of how viruses come into being has been a mystery, one that has deeply perplexed the scientific community. Theorists have proposed three theories of their origin: [4] 

1.      Regression– One theory is that viruses evolve when some free-living organism adopts a parasitic lifestyle, and begins to exploit the genome of its host. The parasite then gradually loses most of its own genetic information, simply because it’s never again used. It’s getting everything it needs from the host. It gets simpler and simpler over its generations, until it becomes a virus.

2.      Co-evolution– A second theory is this: Before any complex life existed on the earth, viruses might have evolved alongside the primitive lifeforms, molecules that first gained the ability to self-replicate. As these early self-replicating patterns came together to form the first cells, viruses co-evolved at the same time to parasitize those cells.

3.      Escape – The third idea is that a bit of genetic information (RNA or DNA), one that exists normally within the cell, gains by mutation the ability to exploit the cell’s replication machinery. Abusing the cell’s machinery, it uses it to reproduce itself. So, the little string starts a parasitic existence inside that cell. Later, after evolving further, it escapes the cell to become an independent virus.

I’ll address each of these theories in turn.

1. The Regression hypothesis sounds plausible. Theorists carefully explored this idea. They know that certain parasites do indeed lose some of their features through Regression, becoming “obligate” parasites. That means they can no longer survive without their hosts. 

To illustrate, the chlamydiae group of organisms—parasites that cause eye inflammation and urinary tract infections (UTIs) in humans—have over the eons become sort of virus-like. The changes are known to have arisen through Regression of more complex parasitic bacteria. Like viruses, Chlamydiae are “obligate intracellular parasites.” They can live only inside cells, and have lost many of their own cellular functions and features. Like viruses, they don’t qualify as complete living things without their host cells. [5]

But despite their dependence, chlamydiae do retain a cellular structure—like their bacterial ancestors, and unlike viruses. And they don’t reproduce the same way viruses do. They replicate by splitting, just as their bacterial ancestors did. Though it is clear Regression has reshaped chlamydiae, then, they are still a long way from being viruses.

Here’s another case theorists have considered: It’s likely that some common cell organelles evolved through Regression. Both mitochondria (the energy-producing organelles in the cells of our bodies) and chloroplasts (the plant organelles that convert sunlight to energy) seem to have arisen in just this way.  

It’s almost certain that both these organelles were originally one-celled parasites. Later they came to live only inside their host cells. They spent so many generations inside their host cells that they gradually lost the ability to live on their own. Parasite and host ended up in a mutually dependent relationship. Again, though, these organelles are a long way from being viruses.

So, although Regression clearly does happen with at least some parasites, there isn’t enough evidence to convince most scientists that viruses originate this way. [6]

2. The Co-evolution hypothesis says host cells and viruses evolved alongside each other, in the same “primordial soup.” Unfortunately, there’s no convincing evidence to prove or disprove this scenario. The events in question are beyond reach, lost in the mists of time. Up to this point, a search for indirect evidence hasn’t turned up anything definitive either. 

A reasonable conclusion is that the Co-evolution hypothesis may hold water. But because so little evidence exists, this hypothesis is only an intriguing possibility.

3. Now we turn to the third origin hypothesis—Escape. According to this theory, says virus expert Arnold Levine, “a portion of the genetic information found in the host cell, or an mRNA copy of this DNA, can gain the ability to replicate itself and then evolve independently of the original host-cell genome. This constitutes an origin event.” [7] A bit of the cell’s own genetic material happens to mutate. By chance, it gains the ability to use the machinery of the cell to create more copies of itself. A normal component of the cell itself has “gone rogue” to become a proto-virus. It has become a self-replicating form that may eventually evolve into a transmissible virus. 

Smoking guns

The Escape hypothesis, say credible experts, has accumulated the most evidence. [8] First, consider the genetic material making up viruses. Many viruses have a genetic core that “is formally and functionally identical” to messenger RNA (mRNA). [9] Messenger RNA, a normal component of cells, is a temporary copy of a gene that is used as a pattern to assemble proteins. According to this hypothesis, a cell automatically translates the mutated RNA into viral proteins, just as with the cell’s own mRNA. 

As virus experts James and Ellen Strauss say, “A reasonable hypothesis for the origin of the RNA viruses is that they began as an mRNA… This proto-virus could then evolve through continued mutation and recombination into something more complex.” [10]

There’s a great deal of intriguing evidence supporting the Escape hypothesis. It comes from the study of simple single-celled organisms including bacteria, archaea, and lower eukarya. [11] Most of these primitive cells contain circular strands of DNA called plasmids. These are strings of genetic information that have gained the ability to replicate and evolve by exploiting the resources of the cell—just as a virus would. 

Though plasmids have gained control of their own replication, they still depend on the host cell for reproduction because, like viruses, they have to use the host’s replication machinery. [12] And as with viruses, a host cell is the natural environment of the plasmid. It can’t survive outside the host, so it’s reasonable to consider plasmids super-simple, “virus-like” parasites.

Plasmids stay inside the cell, but they aren’t integrated into the cell’s own genetic material. They follow their own evolutionary path. As Arnold Levine notes, the fact that they have their own genes “means that they evolve independently of their hosts.” [13]Because they have their own genome, they have an independent identity guiding their evolution—their interests differ from those of their host cell. 

Despite their interests being different, they are still closely connected. Because if the cell dies, the plasmid goes down with the ship. So even though they have separate genomes, their fates are still bound together. In this sense, they are still on the same survival team. Each plasmid has a reason to benefit its cell host, or at least to not harm it. According to virus authority Finbarr Hayes,

• Many plasmids are phenotypically cryptic and provide no obvious benefit to their bacterial host… However, many other plasmids specify traits that allow the host to persist in environments that would otherwise be either lethal or restrictive to growth… Antibiotic resistance is often plasmid encoded and can provide the plasmid-bearing host a competitive advantage… The relative ease with which plasmids can be disseminated among bacteria, compared with chromosome-encoded traits, means that antibiotic resistance can spread rapidly and this has contributed to the dramatic clinical failure of many antibiotics in recent years. [14]

Hangers-on

The relationship between a bacterium and its plasmids can be confusing, so I will offer a fanciful metaphor to clarify it. Let’s say the bacterial cell is like the office building of a large corporation. Most of the people roaming the halls of that building are company employees who have their role in the corporate activity. In this analogy, these company folk are the cell’s own genes. Each employee has a legitimate job there. Each plays a part in the company’s business operations. 

The plasmids used to be on the company payroll, a long time ago. But now they no longer work for the company. Even so, they refuse to leave the building! If challenged by building security, they will have no excuse for being there. They’ve got no business being in that building, because they aren’t part of the company anymore. 

So why are they sticking around? For the best of reasons: it’s cold outside. If they leave the building, they’ll die. But they’ll also die if the company goes out of business. They depend on its success for their very lives. So they can’t afford to interfere with its operations. These hangers-on can best protect their own selfish interests by ensuring that the firm continues to prosper.

For this reason, plasmids often provide benefits to their host cell. One benefit is antibiotic resistance. As researcher C. Kado puts it, “The promiscuous and selfish nature of plasmids is demonstrated by their ability to genetically engineer their host so that the host cell is best able to cope and survive in hostile environments. Survival of the host ensures survival of the plasmid.” [15] Despite their benefit to the company, we shouldn’t consider these ex-staffers altruistic. They have their own selfish interests at heart. It’s just that those interests are best served by helping their host. 

Each of these ex-staffers is on an evolutionary track that’s different from that of the host. One thing all of the plasmids have in common is that they have gotten very good at ducking building security. Each has evolved tricks to avoid being kicked out to the street. 

These hangers-on can be pretty darn aggressive at derailing any attempt to get rid of them. Some of them employ a technique that’s equivalent to planting a bomb in the building, and threatening to set it off if they ever get thrown out.

Really? Yes. Here’s how it works within an actual bacterial cell. It’s called a “toxin/antitoxin” system. Some plasmids produce both a long-lasting poison, and a short-acting antidote to that poison. Suppose the host cell does manage to toss out the plasmid. Then the antidote immediately starts to fade away. But the long-lasting poison is still active. So, the cell inevitably dies after its temporary “victory” over the plasmid. [16] It’s clear these plasmids are not invited guests. They’ve got a stranglehold on their hosts. Insidious!

The plasmids are relating to their host in a disease-like way, much like viruses. Further, some plasmids closely resemble the genomes of full-fledged viruses! So, the distinction between plasmids and viruses can be quite hazy. [17]

Zombie caterpillars

After a plasmid evolves into an actual virus, it loses its incentive to benefit its host. So, viruses often become malignant, harming the host. That isn’t always what happens, though. In special cases a plasmid-turned-virus can continue to be helpful. A spectacular example is parasitic wasps. 

It has long been known that many species of wasp lay their eggs inside caterpillars. The hapless caterpillars become food for the wasp’s developing grubs. Darwin himself seems to have found this wasp characteristic revolting. But Darwin might spin in his grave over a recent discovery that adds a bizarrely sinister twist to the story. 

Scientists have discovered that, as the wasp injects its eggs into the caterpillar, it also injects a virus—a virus that zombifies the caterpillar. From that point forward, each of the poor caterpillar’s actions benefits the parasitic wasp. Science writer Ewen Callaway reports, 

• [T]he wasps have a secret weapon in the form of a dose of virus-like particles that are injected along with the eggs. Not only do these disable the caterpillars’ immune system to stop it attacking the eggs, they also cause paralysis and keep the host from pupating—turning the caterpillar into an eternally youthful larder and nursery for the wasp’s grubs. A closer look at these particles reveals that, although they look like viruses, they contain genetic material from the wasp, which is transcribed into the caterpillars’ DNA—causing production of the very toxins that bring about their downfall. [18]

Callaway speculates that this zombifying virus might have originated, way back in the wasp’s evolutionary history, as a viral infection of the wasp. Perhaps the wasp appropriated and re-engineered the virus for its own use in subduing its caterpillar hosts. [19] Or maybe the virus simply evolved from a plasmid that began as part of the wasp cells’ own DNA. This seems plausible, says science writer Carl Zimmer, because

• … the virus’s DNA resembles some of the wasp’s own genes. The resemblance may actually be hereditary: the virus may descend from a fragment of wasp DNA that mutated into a form that escaped from the normal way genes are copied and stored. [20]

Bizarre as it sounds, the virus may have originated as a snippet of the wasp’s own genes. If true, the wasp and virus are still parts of the same animal. The wasp’s cells routinely produce the carefully tailored virus as an essential part of this parasitization strategy. 

Cutting ties

Several experts see the continuity between cellular genes, plasmids, and viral genomes as “smoking gun evidence,” ample reason to accept the Escape hypothesis. Cellular viruses, they say, begin their existence as normal cellular contents—strands of genetic information that mutate to “go rogue,” gaining the ability to get themselves reproduced over and over. 

And here’s the icing on the cake. When scientists look within simple cells, cells such as bacteria, they find independently evolving plasmids littering the cytoplasm. Nestled within the host cell, but not part of the host DNA, most of the plasmids are not yet complete viruses. But even in this primitive form, they are already clearly virus-like. Because they are independently evolving entities, natural selection gradually “improves” them. Over time, they get better and better—better and better, that is, at serving their own selfish interests. 

As they pass through the generations, plasmids progressively incorporate into their tiny genomes mutations that help them exploit their host. Though these features accumulate in the mindless manner so typical of natural selection, over time the package becomes surprisingly sophisticated. What started out as a barely functioning piece of genetic flotsam ends up having a well-coordinated scheme for self-preservation. Over generations, plasmids come to look more and more like true viruses. 

As long as plasmids depend on the host cell for their reproduction, their interests remain tied to the wellbeing of their host. That tie creates a powerful selection pressure against any plasmid action that would harm the host—and this pressure continues as long as they still need the host. Imagine what would happen, though, if the plasmid could somehow disengage itself—to escape completely from the host. How would that change the course of its evolution?

We don’t have to wonder what would happen. We already know, because some plasmids do jump from one host to another. Smaller plasmids are the most virus-like, moving from one host cell to another in several ways. Some move by “conjugation.” They build tubes between hosts to transfer themselves. And some wrap a membrane around themselves to protect them during a hop between hosts. [21] Some seem to have become full-fledged virions. [22] In these cases the virion particle can be considered a plasmid escape pod. Encased in a protein coat, the ex-plasmid can now maintain its form outside the cell. Having escaped its host, it has become a true virus.

Separated from the host, the ex-plasmid is free to become as “virulent” as it needs to be to reproduce itself with maximum efficiency. As an external agent, it is at liberty to go completely rogue at the host’s expense. And many viruses do exploit their host in a way that heavily burdens or kills it.

How psychology fits within biology

So, it seems that Escape is the most likely origin of biological viruses. Now, the aim of this book is to shift psychology enough that it can help us get a handle on our out-of-control behaviors, for example addictions. Does knowing that viruses arise through Escape help move us toward this goal? Yes, it does. Why? Because virus-like behaviors pop up in pretty much the same way—through Escape. Normal habits turn pathological when they escape their controls. 

To better understand how that happens, we need to get more explicit about psychology’s connection to biology. What follows is a brief overview of that relationship, a sketch the next few chapters will fill in. 

The most basic of all the principles of biology is adaptation. All living things stay alive by adapting, developing their own special ways to survive in their environments. How do they adapt? Through evolution by natural selection. Evolution changes them to fit their circumstances. 

One way of talking about this is that living things accumulate survival wisdom through natural selection. Some theorists call the evolution of wisdom “species learning.” [23] As a species evolves, it stores its accumulated wisdom in its genes, patterns encoded in the DNA of its cells. The genes are a resource shared by every animal of that species. 

Even lower animals (those that can’t learn) have to apply their stored wisdom with sensitivity if they are to stay alive. They have to use the species’ wisdom in a way that fits what’s going on in the here and now. A single-cell bacterium, for example, activates genes differently under different conditions, in ways most likely to keep it alive. Simple multicelled animals do the same. We apply the word “instinctive” to the behavior of these simple animals, because their acts flow directly from their inherited, species-wide wisdom. For this reason, their behavior is pretty rigid. All the individuals of a lower species end up doing almost exactly the same thing, like little robots.

But higher animals are different. Individuals of those more capable species tailor their instinctual drives to precisely match their activity to their differing circumstances, moment-by-moment. They accomplish this through their learned habits. To conduct its business, each higher animal accumulates its own individual collection of useful habits. Then the animal selectively activates its habits according to what it needs in the moment. What a great system! As theoretical immunologist Irun Cohen phrases it, higher animals’ ability to use habits “extends the evolutionary germ-line learning of the species.” [24] 

Every species, no matter how simple, encodes its wisdom as a collection of genes. And every individual animal of that species uses that collection to survive. Lower animals express their instincts without much variability. That direct, unvarying expression is what makes them look robotic. But higher animals individually customize their inherited instincts into a collection of learned habits. Their made-to-order habits give them much greater flexibility than lower animals. But that very flexibility introduces a vulnerability that lower animals don’t have. What’s the vulnerability? Their learned habits can go rogue, escaping their governance. But… what governance are we talking about?

The governance of the self

Whether it’s the species as a whole, or a single individual of a species, stored wisdom is activated and applied under the guidance of “a self.” What’s a self? It’s a kind of inventory the animal uses to distinguish things that sustain its life from things that aren’t good for it. The immune system is an agent of the self, actively protecting the animal. Immunity is a topic of tremendous importance, for both animal bodies and animal behavior. We’ll talk a lot more about immunity in later chapters.

It’s characteristic of every living thing that all the elements of its collected wisdom work together cooperatively. Each of the animal’s genes, for example, evolves to work seamlessly with all the other genes in the collection. Taken together, all the species’ genes form an integrated whole. The same principle applies to a higher animal’s collection of habits. As the animal expresses its habits, they evolve under the guidance of the self to work well with each other. 

It’s natural selection that brings about the co-adaptation of those elements. The elements making up a living thing vary over time. Selection of variants is actively managed by the animal’s self. Variants that work well with all the others are selected. Those that don’t fit end up rejected. 

Here’s a key question: How are the variants selected? Where the animal’s genes are concerned, death does the selection. A variant that doesn’t fit won’t work well with the others, and is likely to prove fatal. Death removes that variant from the population, because the animal doesn’t pass it to the next generation. Where habits are concerned, though, the animal’s feelings make the selection. [25] When a variant habit doesn’t work well, the animal is dissatisfied and frustrated, left unfulfilled. So, the animal doesn’t repeat that variant—if it can avoid repeating it. [26]

Every animal has to manage variant elements as they crop up. Some variants don’t fit into the animal’s scheme for staying alive, and are quickly rejected by the active arm of the self, the animal’s immune functions. But certain conditions increase the chances that a bad variant will entirely escape the governance of the self. We can apply the label “rogue” to an out-of-control variant, one that has dodged immunity. 

A rogue is not necessarily harmful in itself. And as we have seen, a cell’s rogue plasmids are sometimes even beneficial. But because a rogue continues to evolve outside the governance of the self, it has the potential to become parasitic. That is, it may further evolve to use the animal as its host, in a virus-like way. Any rogue, in other words, could evolve into a parasitic disease.

Only biological evolution can change a cell’s biological genome. But our personal collection of instincts and habits functions as if it were a  “behavioral genome.” [27] Individual humans, like every other higher animal, can expand or alter their behavioral genome “on the fly” as their personal circumstances require. Our ability to embellish our individual habits through learning is what gives us our characteristic behavioral flexibility. But it also opens us to the rise of rogue habits, which may turn into stubbornly persistent parasitic behaviors like alcoholism and anorexia. More about this in later chapters.

The mystery of awareness

Here’s something quite interesting about habits, something that’s a clue to the mystery of conscious awareness. As I said, the selection of habit variants happens through the animal’s feelings. Higher animals make their choices according to their subjective sense of what’s “good for it” and what’s “bad for it.” That subjective sense suggests a role for awareness in habit construction. 

In fact, careful research shows that conscious awareness is essential for habit formation. The evidence says that new habits simply can’t be constructed without awareness. And once a habit is firmly established, it invariably fades from awareness. We know that, once a habit is firmly in place, we can engage in very complex behavior with zero awareness of what we are doing. Further, existing habits can’t be changed unless they are brought back into awareness! [28] Consciousness, it seems, is closely associated with the moment-by-moment adaptation of our stored wisdom—both our inherited drives and our personal collection of habits—to our current circumstances.

Knowing the intimate connection between awareness and habit formation leads us to a conclusion that’s immensely important. It tells us how habits can go rogue, defying our control. If an established habit can evade our awareness, it can persist indefinitely—even if it is clearly harmful. If we think carefully about this, we will begin to understand why every addiction, without exception, is shrouded in the crippling distortion of awareness we call denial. Addiction is a rogue habit that persists because it has gained the ability to dodge our awareness. Further, every other stereotypic, malignant, self-replicating pattern in our individual and collective lives persists for the very same reason.

Virus-like habits

And now we come to the point of this chapter. There’s an outstanding reason for looking closely at the way biological viruses come into being. Rogue habits become parasitic, virus-like habits in much the same way that plasmids become parasitic viruses. It’s just that plasmids evolve into viruses over the course of many animal generations, where habits can become virus-like during the lifetime of a single individual. 

To more deeply understand how a habit can escape its controls, it helps to know what habits really are, and how they actually work. I’ll present a useful perspective on habits in the next chapter.

What’s in a name?

But before the end of this chapter, we should consider the origin of the word virus. It comes from a Latin word for “poison.” [29] In medical use, the word “virus” historically had an entirely generic meaning. It referred to the cause of any disease transmissible from one person to another. This sense of the word persists even now in the term “virulent,” which means highly infectious.

In 1892 Russian scientist Dmitri Ivanosky discovered that juices from diseased tobacco plants retained the power to infect other plants even after the juice had passed through a very fine filter. The smallest infectious agents then known were bacteria. But a bacterium is large enough that this fine filter would remove it. This meant that the mysterious agent of infection had to be much smaller than a bacterium. 

So, scientists labeled the unknown cause of the tobacco disease “a filterable virus,” meaning literally “an infectious agent that can pass through a filter.” In time they streamlined the clumsy term “filterable virus” to simply “virus.” It was in this way that the word came to its modern meaning. The word “virus” now refers to a parasitic nucleotide string able to hop from one host to another. [30]

Sometime in the mid-1970s, as computer hackers began writing infectious code that could spread from one machine to another, their malicious little programs were tagged with the fanciful name “computer virus.” That seemed as good a handle as any, because the way they spread was reminiscent of the way biological viruses spread. There were objections to this term, though, because obviously computer viruses are not real viruses. Some thought the label would create confusion. But in truth there was already a lot of confusion about what a “real” virus might be. 

These days the word “virus” has a tidy, scientific ring. That scientific aura might lead us to think a virus is something well-defined and well-understood. But that’s just not the case. 

Theorist Luis Villareal points out that there are many kinds of viruses, and a menagerie of other virus-like “things.” Some of these have most of the characteristics of viruses. As researchers discover more and more virus-like things, they keep making up new names for them. But they can’t agree on the difference between a “real” virus and a thing that’s only “virus-like.” 

Villareal has expressed frustration at the “babble-like” proliferation of labels for these things. We can eliminate some of the confusion, he says, by getting back to basics. He proposes that we think of a virus in a more generic way as “a genetic string that can parasitize its host cell and be maintained or reproduced.” [31] He concedes that this definition is likely to include agents that some scientists would rather not consider “real” viruses. 

Villareal’s “return to basics” point is well taken. But we can widen our thinking about self-reproducing processes even further. As Villareal stresses, the word “virus” is just a label. We can choose to reserve that word only for biological viruses based on DNA or RNA. Or we can use the concept behind the word in a broader and more flexible way. We can use it as a metaphor, a way to widen our understanding of self-replicating structures operating within a variety of media.

Villareal’s virus definition is almost generic. It even comes close to covering virus-like computer programs. We only have to change two words in his definition to read “a code string that can parasitize its host program and be maintained or reproduced.” That’s a fair description of a computer virus. We could change the same two words to get “a behavior string that can parasitize its host animal and be maintained or reproduced.” Now it becomes a fair description of a behavioral virus. 

We can call a self-reproducing string of behaviors a “behavioral virus.” Or we could invent some other word to describe them. The label isn’t what’s important. What’s important is understanding the concept. 

We need to grasp how a string of behaviors can reproduce itself by exploiting the resources of the behaving host—and especially how these patterns develop their ability to persist despite their destructive impact. It does help, of course, if the label we choose provides a clue about what’s going on. Just as the term “computer virus” drops hints as to how these little programs propagate, “behavioral virus” helps us see how this kind of rogue habit reproduces itself.

Summary

·    Viral-like patterns likely come into being within a cell when normal cellular material—for example, messenger RNA or a portion of genomic DNA—mutates to a form with the ability to reproduce itself. 

·    Once engendered, a viral process evolves independently of the host cell. When it does, its interests diverge from those of the host cell.

·    Strong evidence of the origin of viruses is the presence, within bacterial cells, of independently reproducing genetic strands called plasmids.

·    The genesis of biological viruses leads to speculation that behavioral viruses arise similarly in higher animals. Habits can “go rogue” if they escape the governance of “the self,” gaining control of their own reproduction. Having escaped, they may begin to relate to us as parasite to host.

·    Understanding the relationship between psychology and biology provides clues about the role of conscious awareness in learning.

[Post Episode] 

Thank you for your interest in this episode, Healing Psychology Part F – Viral Origins. Additional information is available on the website, Whiteheadbooks dot com, where you can also find credits for the music tracks you heard.

The Healing Psychology series will continue with readings of additional chapters of the book. The title of the next part is “The Drive/Habit System.” In Part G we’ll look closely at nature’s system for creating and maintaining normal habits. If we can understand how habits are normally created, we can better understand how the process can go wrong. In fact, grasping the Drive/Habit system shows how, why, and under what conditions malignant habits arise. 

Please join us!

[Music credits] 

1.     “145” -  Written and performed by Tom Whitehead.
2.     “Voyage of Discovery” - Written and performed by Tom Whitehead.

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[1] Durzyńska J and Goździcka-Józefiak A. Viruses and cells intertwined since the dawn of evolution. Virology Journal, 2015, 12, 169.
[2] Of course, the behavior in question does flow from a physical form – the body of the host animal. But that physical form belongs entirely to the host, and doesn’t perpetuate parasitic habits on its own.
[3] Biologists (and most psychologists) assume that habitual behavior – including perceptual processes – is based upon the interaction of chemicals within the brain.
[4] This information is drawn from a work by virus expert Arnold J. Levine:  [Levine AJ. Viruses. Scientific American Library (A division of HPHLP), New York, 1992].
[5] Becker Y. Chlamydia. Chapter 39 of Medical Microbiology (4th edition), Samuel Baron, editor. 1996, The University of Texas Medical Branch at Galveston. Available online at https://www.ncbi.nlm.nih.gov/books/NBK8091/
[6] Levine AJ, 1992. Page 198.
[7] Levine AJ, 1992. Pages 198-199.
[8] Forterre P, Krupovic M. The origin of virions and virocells: The escape hypothesis revisited. Chapter in Viruses: Essential Agents of Life (G. Witzany, ed.), Pages 43-60. Published online September 25, 2012. Page 43.
[9] Anonymous. Viruses. Article on MIT website. Available online at http://web.mit.edu/7.01x/7.012/pdfs/Viruses_2.pdf
[10] Strauss JH, Strauss EG. Viruses and Human Disease. Academic Press, 2002. Page 105.
[11] Bacteria, archaea, and eukarya are the three domains (major groupings) of life on planet earth. We humans are eukaryotes, as are all other complex multicelled animals. Bacterial and archaeal cells are simpler life-forms, usually consisting of a single cell. Plasmids are common within these simpler cells. See [Hayes F. The function and organization of plasmids. Chapter in Casali N and Presto A, E. Coli plasmid vectors: Methods and applications. Methods in Molecular Biology, 2003, 235, 1-5. Page 1.]
[12] Ashwathi P. Plasmids in Bacteria: Properties, Types and Replication. Article on website Biology Discussion. Available at http://www.biologydiscussion.com/bacteria/plasmids-in-bacteria-properties-types-and-replication/51146
[13] Levine AJ, 1992. Page 199.
[14] Hayes F. The function and organization of plasmids. Chapter in Casali N and Presto A, E. Coli plasmid vectors: Methods and applications. Methods in Molecular Biology, 2003, 235, 1-5. Page 3.
[15] Kado CI. Origin and evolution of plasmids. Antonie Van Leeuwenhoek, 1998,73, 1, 117-126. Page 117
[16] Kroll J, Klinter S, Schneider C, Voss I, Steinbuchel A. Plasmid addiction systems: Perspectives and applications in biotechnology. Microbial Biotechnology, 2010, 3, 6, 634-657. Pages 634-635. Kroll et al say, “Diverse mechanisms have been evolved to ensure stable maintenance of plasmids in cells… preventing the survival of plasmid-free cells due to selective killing. The principle of [toxin/antitoxin] systems is the counteraction of two proteins from which one is a stable toxin and the other is an unstable antitoxin.” Page 635.
[17] Levine AJ, 1992. Pages 200-201.
[18] Callaway E. Ancient virus gave wasps power over caterpillar DNA. New Scientist. Online article, February 13, 2009. Available at www.newscientist.com/articles/dn16597-ancient-virus-gave-wasps-power-over-caterpillar
[19] Bezier A, et al. Polydnaviruses of braconid wasps derived from an ancestral nudivirus. Science, 2009, 323, 5916, 926-930. Page 926.
[20] Zimmer C. Parasite Rex: Inside the bizarre world of nature's most dangerous creatures. Simon & Schuster, New York, 2000. Page 77.
[21] See [Smillie C, Garcillán-Barcia MP, Francia MV, Rocha EPC. Mobility of Plasmids. Microbiology and Molecular Biology Reviews, 2010, 74, 3] and  [Erdmann S, Tschitschko B, Zhong L, Raftery MJ, Cavicchioli R. A plasmid from an Antarctic haloarchaeon uses specialized membrane vesicles to disseminate and infect plasmid-free cells. Nature Microbiology, 2017, 2, 10, 1446-1455]
[22] Forterre P, Da Cunha V, Catchpole R. Plasmid vesicles mimicking virions. Nature Microbiology, 2017, 2, 10, 1340–1341
[23] Immunologist Irun Cohen uses this term in his delightful book, Tending Adam’s Garden [Cohen IR, 2004].
[24] Cohen IR, 2004. Page 86.
[25] Psychologist Edward L. Thorndike formalized the principle as “Thorndike’s Law” of learning. More about this later.
[26] Under some conditions they can’t avoid repeating unsatisfying variants. And this increases the likelihood of disease. We’ll discuss this in some detail later.
[27] It was William James who said, “All our life, so far as it has definite form, is but a mass of habits - practical, emotional, and intellectual - systematically organized for our weal or woe, and bearing us irresistibly toward our destiny, whatever the latter may be." [James W. The laws of habit. Chapter 8 of Talks to Teachers on Psychology: and To Students on Some of Life's Ideals. W.W. Norton, 1958, page 56.] Available online at https://www.uky.edu/~eushe2/Pajares/tt8.html
[28] Dehaene S and Naccache L. Towards a cognitive neuroscience of consciousness: Basic evidence and a workspace framework. Cognition, 2001, 79, 1-37. Pages 12-13. Though the connection between awareness and habit assembly has direct implications for consciousness research, it is mostly ignored by theorists!
[29] That Latin word can be traced back to a much older Sanskrit word “visham,” which also means poison.
[30] Nathanson N. Viral Pathogenesis and Immunity. Academic Press, 2007. Page 6.
[31] Villareal LP. Origin of Group Identity: Viruses, Addiction and Cooperation. Springer Science and Business Media, 2008. Page 51.