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The mystery of the origin of viruses
The mystery of the origin of viruses

Video: The mystery of the origin of viruses

Video: The mystery of the origin of viruses
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Viruses are hardly alive. However, their origin and evolution are even less understood than the emergence of "normal" cellular organisms. It is still unknown who appeared earlier, the first cells or the first viruses. Perhaps they always accompanied life, like a disastrous shadow.

The problem is that viruses are nothing more than fragments of the genome (DNA or RNA) enclosed in a protein coat. They leave no traces in the fossil record, and all that remains to study their past is modern viruses and their genomes.

Comparing, finding similarities and differences, biologists discover evolutionary links between different viruses, determine their most ancient features. Unfortunately, viruses are unusually variable and varied. Suffice it to recall that their genomes can be represented by chains of not only DNA (as in our country and, for example, herpes viruses), but also a related RNA molecule (as in coronaviruses).

The DNA / RNA molecule in viruses can be single or segmented into parts, linear (adenoviruses) or circular (polyomaviruses), single-stranded (anelloviruses) or double-stranded (baculoviruses).

Influenza virus A / H1N1
Influenza virus A / H1N1

Visual science Influenza A / H1N1 virus

The structures of viral particles, the peculiarities of their life cycle and other characteristics, which could be used for ordinary comparison, are no less diverse. You can read more about how scientists get around these difficulties at the very end of this post. For now, let's remember what all viruses have in common: they are all parasites. Not a single virus is known that could carry out metabolism on its own, without using the biochemical mechanisms of the host cell.

No virus contains ribosomes that could synthesize proteins, and no one carries systems that allow the production of energy in the form of ATP molecules. All this makes them obligate, that is, unconditional intracellular parasites: they are unable to exist on their own.

It is not surprising that, according to one of the first and most well-known hypotheses, cells first appeared, and only then the whole diverse viral world developed on this soil.

Regressively. From complex to simple

Let's take a look at rickettsia - also intracellular parasites, albeit bacteria. Moreover, some parts of their genome are close to DNA, which is contained in the mitochondria of eukaryotic cells, including humans. Apparently, both of them had a common ancestor, but the founder of the "line of mitochondria," infecting the cell, did not kill it, but was accidentally preserved in the cytoplasm.

As a result, the descendants of this bacterium lost a mass of more unnecessary genes and degraded to cellular organelles that supply the hosts with ATP molecules in exchange for everything else. The "regressive" hypothesis of the origin of viruses believes that such degradation could have happened to their ancestors: once completely full-fledged and independent cellular organisms, over billions of years of parasitic life, they simply lost everything superfluous.

This old idea has been revived by the recent discovery of giant viruses such as pandoraviruses or mimiviruses. They are not only very large (the particle diameter of the mimivirus reaches 750 nm - for comparison, the size of the influenza virus is 80 nm), but they also carry an extremely long genome (1.2 million nucleotide links in mimivirus versus several hundred in common viruses), encoding many hundreds of proteins.

Among them there are also proteins necessary for copying and "repair" (repair) of DNA, for the production of messenger RNA and proteins.

These parasites are much less dependent on their hosts, and their origin from free-living ancestors looks much more convincing. However, many experts believe that this does not solve the main problem - all "additional" genes could appear from giant viruses later, borrowed from their hosts.

After all, it is difficult to imagine a parasitic degradation that could go so far and affect even the form of the carrier of the genetic code and lead to the emergence of RNA viruses. It is not surprising that another hypothesis about the origin of viruses is equally respected - the completely opposite.

Progressive. From simple to complex

Let's take a look at the retroviruses, whose genome is a single-stranded RNA molecule (for example, HIV). Once in the host cell, such viruses use a special enzyme, reverse transcriptase, converting it into ordinary double DNA, which then penetrates into the "holy of holies" of the cell - into the nucleus.

This is where another viral protein comes into play, integrase, which inserts the viral genes into the host's DNA. Then the cell's own enzymes begin to work with them: they produce new RNA, synthesize proteins on their basis, etc.

Human Immunodeficiency Virus (HIV)
Human Immunodeficiency Virus (HIV)

Visual scienceHuman Immunodeficiency Virus (HIV)

This mechanism resembles the reproduction of mobile genetic elements - DNA fragments that do not carry the information we need, but are stored and accumulated in our genome. Some of them, retrotransposons, are even capable of multiplying in it, spreading with new copies (more than 40 percent of human DNA consists of such "junk" elements).

For this, they may contain fragments encoding both key enzymes - reverse transcriptase and integrase. In fact, these are almost ready-made retroviruses, devoid of only a protein coat. But its acquisition is a matter of time.

Embedding in the genome here and there, mobile genetic elements are quite capable of capturing new host genes. Some of them might be suitable for capsid formation. Many proteins tend to self-assemble into more complex structures. For example, the ARC protein, which plays an important role in the functioning of neurons, spontaneously folds in free form into virus-like particles that can even carry RNA inside. It is assumed that the incorporation of such proteins could occur about 20 times, giving rise to large modern groups of viruses that differ in the structure of their envelope.

Parallel. Shadow of life

However, the youngest and most promising hypothesis turns everything upside down again, assuming that viruses appeared no later than the first cells. A long time ago, when life had not yet gone so far, the proto-evolution of self-replicating molecules, capable of copying themselves, proceeded in the "primordial soup".

Gradually, such systems became more complex, transforming into larger and larger molecular complexes. And as soon as some of them acquired the ability to synthesize a membrane and became proto-cells, others - the ancestors of viruses - became their parasites.

This happened at the dawn of life, long before the separation of bacteria, archaea and eukaryotes. Therefore, their (and very different) viruses infect representatives of all three domains of the living world, and among viruses there can be so many RNA-containing ones: it is RNAs that are considered "ancestral" molecules, self-replication and evolution of which led to the emergence of life.

The first viruses could be such "aggressive" RNA molecules, which only later acquired genes encoding protein envelopes. Indeed, it has been shown that some types of shells may have appeared even before the last common ancestor of all living organisms (LUCA).

However, the evolution of viruses is an area even more confusing than the evolution of the entire world of cellular organisms. It is very likely that, in their own way, all three views on their origin are true. These intracellular parasites are so simple and at the same time diverse that different groups could appear independently of each other, in the course of fundamentally different processes.

For example, the same giant DNA-containing viruses could arise as a result of the degradation of ancestral cells, and some RNA-containing retroviruses - after "gaining independence" by mobile genetic elements. But it is possible that we owe the appearance of this eternal threat to a completely different mechanism, not yet discovered and unknown.

Genomes and genes. How the evolution of viruses is studied

Unfortunately, viruses are incredibly volatile. They lack systems for repairing DNA damage, and any mutation remains in the genome, subject to further selection. In addition, different viruses that infect the same cell easily exchange DNA (or RNA) fragments, giving rise to new recombinant forms.

Finally, generational change occurs unusually quickly - for example, HIV has a life cycle of only 52 hours, and it is far from the shortest lived. All these factors provide the rapid variability of viruses, which greatly complicates the direct analysis of their genomes.

At the same time, once in a cell, viruses often do not launch their usual parasitic program - some are designed this way, others because of an accidental failure. At the same time, their DNA (or RNA, previously converted into DNA) can integrate into the host's chromosomes and hide here, being lost among the many genes of the cell itself. Sometimes the viral genome is reactivated, and sometimes it remains in such a latent form, being passed down from generation to generation.

These endogenous retroviruses are believed to account for up to 5-8 percent of our own genome. Their variability is no longer so great - cellular DNA does not change so rapidly, and the life cycle of multicellular organisms reaches tens of years, not hours. Therefore, the fragments that are stored in their cells are a valuable source of information about the past of viruses.

A separate and even younger area is the proteomics of viruses - the study of their proteins. After all, after all, any gene is just a code for a certain protein molecule required to perform certain functions. Some "fit" like Lego pieces, folding the viral envelope, others can bind and stabilize viral RNA, and still others can be used to attack the proteins of an infected cell.

The active sites of such proteins are responsible for these functions, and their structure can be very conservative. It retains great stability throughout evolution. Even individual parts of genes can change, but the shape of the protein site, the distribution of electric charges in it - everything that is critical for the performance of the desired function - remains almost the same. By comparing them, one can find the most distant evolutionary connections.

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