(ORDO NEWS) — Scientists still do not know what came first – viruses or cells on which they parasitize.
It is unlikely that viruses can be called alive. However, their origin and evolution are even less understood than the emergence of “normal” cellular organisms. It is still unknown who appeared first, the first cells or the first viruses. Perhaps they have always accompanied life, like a deadly 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 are 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 diverse. Suffice it to recall that their genomes can be represented by chains of not only DNA (like ours and, for example, herpesviruses), but also a related RNA molecule (like 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 A/H1N1 virus
No less diverse are the structures of viral particles, the features of their life cycle, and other characteristics that could be used for a normal comparison.
You can read more about how scientists get around these difficulties at the very end of this note. In the meantime, let’s remember what all viruses have in common: they are all parasites. No 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 none carry systems that allow energy to be generated 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 famous hypotheses, cells first appeared, and only then the entire diverse viral world developed on this basis.
Regressively. From complex to simple
Let’s take a look at Rickettsia, which are also intracellular parasites, although they are bacteria. At the same time, 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”, having infected the cell, did not kill it, but accidentally remained in the cytoplasm. As a result, the descendants of this bacterium lost a lot of unnecessary genes and degraded into cellular organelles that supply ATP molecules to their hosts 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 complete and independent cellular organisms, over billions of years of parasitic life, they simply lost everything superfluous.
This old idea has been given a fresh breath by the recent discovery of giant viruses such as pandoraviruses or mimiviruses.
They are not only very large (the diameter of a mimivirus particle reaches 750 nm – for comparison, the size of the influenza virus leaves 80 nm), but also carry an exceptionally long genome (1.2 million nucleotide units in a mimivirus versus several hundred in ordinary 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 is much more convincing. However, many experts believe that this does not solve the main problem – all the “additional” genes could appear in the giant viruses later, borrowed from the hosts.
After all, it is hard to imagine parasitic degradation that could go so far as to 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, which is completely opposite, enjoys no less respect.
Progressively. From simple to complex
Let’s take a look at 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, turning it into a regular double DNA, which then enters the “holy of holies” of the cell – the nucleus.
This is where another viral protein, integrase, comes into play, 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 based on them, etc.
Human Immunodeficiency Virus (HIV)
This mechanism is reminiscent of 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 able to multiply in it, spreading with new copies (human DNA consists of such “junk” elements by more than 40 percent).
To do this, they may contain fragments encoding both key enzymes – both reverse transcriptase and integrase. In fact, these are almost ready-made retroviruses, devoid of only a protein shell. But its acquisition is a matter of time.
Embedded 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 be carried inside RNA. It is assumed that the inclusion 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, suggesting that viruses appeared no later than the first cells. A long time ago, when life had not yet gone that far, the proto-evolution of self-replicating molecules, capable of copying themselves, proceeded in the “primordial soup”.
Gradually, such systems became more complex, turning into ever 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 the existence of life, long before the separation of bacteria, archaea and eukaryotes.
Therefore, their own (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, the 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 coats. Indeed, it has been shown that some types of shells may have appeared before the last common ancestor of all living organisms (LUCA).
However, the evolution of viruses is an area even more complicated than the evolution of the entire world of cellular organisms. It is very likely that all three views on their origin are valid in their own way.
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 have arisen as a result of degradation of ancestral cells, and some RNA-containing retroviruses could have arisen after “gaining independence” by mobile genetic elements.
But it is possible that we owe the emergence of this eternal threat to a completely different mechanism, as yet undiscovered and unknown.
Genomes and genes. How to study the evolution of viruses
Unfortunately, viruses are incredibly volatile. They lack systems for repairing (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, generating new recombinant forms.
Finally, generational change is unusually fast – for example, the life cycle of HIV is only 52 hours, and it is far from the shortest-lived. All these factors ensure 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 arranged this way, others – due to a random failure.
At the same time, their DNA (or RNA, previously converted into DNA) can be integrated into the host’s chromosomes and hide here, lost among the many genes of the cell itself. Sometimes the viral genome is reactivated, and sometimes it remains in such a latent form, passing 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 remain in their cells serve as 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, in the end, any gene is just a code for a certain protein molecule necessary to perform certain functions. Some “join” like Lego pieces, folding the viral shell, others can bind and stabilize viral RNA, and others can be used to attack the proteins of an infected cell.
The active sites of such proteins are responsible for performing these functions, and their structure can be very conservative. It retains great stability throughout evolution.
Even individual sections of genes can change, but the shape of the protein site, the distribution of electric charges in it – everything that is critical for performing the desired function – remains almost the same. Comparing them, one can find the most distant evolutionary connections.
Contact us: [email protected]