Where does the virus come from?

155

Where does the virus come from ? 1st of all, anyone who understand evolution should know that as long as you go back up, any two living things can be traced back to a common ancestor

And the ancestors can continue to trace back to the common ancestor of the ancestors, and finally build a tree that can cover the evolution of all living beings in ancient and modern times tree.

However, the virus does not seem to be on this tree. The structure of most viruses is very simple. Basically, a shell made of protein encloses some genetic material.

Usually it is no different from a dead thing. Once a cell is infected, they inject their own genes into the host cell and use the host cell to replicate themselves. Create new viruses. 

This strange way of life makes it difficult for us to place it anywhere in the tree of evolution.

Are viruses biological ? Where do they come from?

Below, we will look at three hypotheses about the origin of the virus.

Hypothesis 1: The vengeful soul of ancient life

The story of the virus may start from ancient times. On that lifeless earth, the ocean occupies most of the world, and under the endless sea is continuous volcanic activity for hundreds of millions of years. 

By some coincidence, the first batch of organic macromolecules were produced in the sea water, which ignited the spark of life.

Gradually, some large molecules, such as RNA, DNA, and proteins, begin to replicate themselves independently or cooperatively. This stage can be called “molecular life”. 

However, in a peaceful molecular life, a different kind has emerged, that is, some molecular life, including the nearest common ancestor “Luca” (LUCA) of all living creatures, have developed a structure that changes the law of life. That is the cell. 

Cells with membrane structure can better protect the delicate core macromolecules such as RNA and protein, which greatly enhances the adaptability of these organisms, which means that they will rub the original molecular life on the ground.

hypothesis (The Virus-First Hypothesis)

And there is a hypothesis (The Virus-First Hypothesis) that viruses are the remains of the world of primitive molecular life.

They create a parasitic lifestyle at the last moment, and in turn use the enemy’s cellular structure, just like a group of ancient The soul of vengeance makes an eternal struggle against the race that seizes its homeland.

This hypothesis was once very popular. After all, the structure of viruses is so simple, even crude, and the difference between them and cell life is so huge.

The more solid evidence comes from the “virusoid”, which is an RNA molecule. Virus can not directly infect cells, but it can infect viruses. To be precise, when certain viruses infect cells, they can free ride to replicate and spread themselves, which can cause some diseases such as human hepatitis D. .

However, this hot-blooded virus origin story is no longer so perfect with the deepening of molecular biology research…

Hypothesis 2: “Defection” gene

Can genes with big eyebrows and big eyes betray? Yes, in this hypothesis (The Progressive Hypothesis) , genes do everything to let themselves pass on.

A small fragment of circular DNA called “plasmid” is widespread in bacteria. These genes are basically a group of temporary workers. The bacteria can absorb them from the environment for their own use, and they can also be driven away at any time. .

So in the long evolution, some plasmids have learned one thing: we don’t want to work all our lives! These plasmids changed from wage earners to twenty-five kids, and in turn hijacked their bacterial bosses, taking away all the bacteria’s nutrients to replicate themselves. Over time, some plasmids become viruses.

The cells and bacteria of human beings and all animals and plants are very different. We are all “eukaryotes”. There are no bacteria-like plasmids in the cells, but there are still some genes that are ready to move. 

They refused to stay on the chromosome, but jumped left and right in the nucleus, running to this chromosome and then to that chromosome. However, these mischievous genes have a fairy-style name- transposon.

According to molecular biology tests, many transposons have genetic sequences very similar to viruses, and the mechanisms by which the two integrate themselves into the host cell chromosomes are also highly similar. 

In particular, the “virus-like retrotransposon” (Retrotransposon) is similar to some viruses to an egregious degree. The only difference is that these transposons cannot migrate between cells like viruses.

However, the life experience of viruses is still confusing here, because they do not follow the evolutionary pattern of ordinary organisms at all.

The general process of virus infection is: inject your own genes into host cells, then use the host cells to replicate their genes, and make all the materials needed to build the virus particles, and finally control the cells to transfer the various parts of the virus particles together with the virus genes Packaged together into new virus particles, released to infect other cells.

But in this process, viruses are exchanging genes with various organisms all the time.

For example, when a virus instructs host cells to package virus particles, it sometimes packs some host cell DNA in one piece, or accidentally leaves a little bit of its own genes in the host cell. 

There is a gene in mammals that prevents the maternal immune system from attacking the fetus. It is a virus that accidentally landed in our cells for more than 100 million years. When the virus spreads across species, it often results in the transfer of genes from one species to another. Therefore, the “transgenic” matter is left over by nature.

However, it is precisely because the genetic modification of the virus is so frequent that people have to rethink, is the virus really a gene of defect? Have we mistaken the logical relationship from the beginning? Those transposons, maybe not their own genes that are disturbed, but viral genes accidentally left in the cell?

Hypothesis 3: Viruses may be sinking cellular organisms

After entering the 21st century, a series of discoveries began to make scientists more aware of the possibility of the origin of the virus.

In 2003, scientists discovered a very unreasonable virus-“Mimivirus” (Mimivirus), this virus has a size of 0.4 to 0.5 microns, and looks almost like bacteria under a microscope. 

The coronavirus that caused this epidemic is considered to be a relatively large type of virus, and the size is less than 0.1 micron.

In 2008, scientists discovered the second major virus and named it “Mamavirus”. Since then, “Giant Virus” (Giant Virus) has appeared one after another in the field of vision of human beings, until 2013 The “Pandoravirus” discovered in 1999 even brushed the record of the largest virus to more than 1 micron.

Since then, the boundaries between viruses and certain single-celled organisms have become blurred. For example, the structure and genes of “pseudoviruses” are very similar to a type of single-celled organisms called “archaea”.

The only difference is that Bacterial viruses have lost some of the key genes that complete cell division autonomously, so they have to parasitize the cells of other organisms and use the cells of the host to grow and reproduce.

hypothesis of the origin of viruses

So there is the third hypothesis of the origin of viruses (The Regressive Hypothesis), which believes that viruses are essentially fallen creatures. In the long-term parasitic life, some single-celled organisms gradually degenerate most of the cell structure, and eventually become this kind of living dead, and the likes of mimic viruses are archaea that have just begun to degenerate.

The virus has left a deep mark

The virus has left a deep mark So, should the virus be an ancient vengeful soul, a gene that defected, or a fallen creature? These three hypotheses are reasonable, but there are also unexplainable problems. Perhaps the origin story of the virus is far more complicated than all these hypotheses, and may not even have the only source.

We may never know where the virus came from, but the virus has really left a deep imprint on our evolution.

Due to the extremely powerful mutation ability of viruses, we will never be able to predict when and where a virus that is fatal to us will appear. In the end, many creatures have to adopt some methods to defeat mutation by mutation.

For example, sexual reproduction. The most direct consequence of sexual reproduction is that the genes of each of our offspring can be disrupted and rearranged, as far as possible to protect all offspring from being caught by a virus. 

The arms race between viruses and organisms has always been the strongest driver of evolution, and viruses have also broken the barriers of reproductive isolation, allowing genes to flow in different organisms.

Therefore, although viruses do not belong to any branch of the tree of evolution, they are like the fireflies and ghosts surrounding the tree of evolution, leaving their own traces everywhere on this tree.

So why do deadly viruses always come from wild animals? Let us analyze it from the perspective of evolution.

The “best” virus does not cause too serious symptoms (otherwise it will kill the host and be dead), but it must not be too mild (after all, the host is often parasitic with other viruses at the same time, so it should be used when grabbing resources. Ruthless still has to play). 

Therefore, in the long evolution, this kind of game will prompt the virus to finally reach a certain tacit agreement with the host. For example, humans and rhinoviruses that may cause the common cold belong to this relationship.

However, the virus will mutate, and some mutations will cause the host of the virus to change. 

If there is no long-term tacit understanding between the virus and the new host, there will be a problem of “no light or serious attack”, and some of them will cause deadly diseases to the host if they are particularly severe.

In the long-term evolution, humans have reached a perfect tacit understanding with the viruses that have been with them since ancient ancestors, and the viruses that came from domestic animals, such as measles, influenza, etc.

are not perfect, but somewhat tacitly. It rarely causes a serious epidemic. Only viruses that come from wild animals have nothing to do with us, so almost all diseases that cause the great plague come from wild animals.

Reference materials:

• 1.Wessner, DR (2010). The origins of viruses. Nature Education, 3(9), 37.
• 2. Suchard, MA, Lemey, P., Baele, G., Ayres, DL, Drummond, AJ, & Rambaut, A. (2018). Bayesian phylogenetic and phylodynamic data integration using BEAST 1.10. Virus evolution, 4(1) , vey016.
• 3.Duffy, S. (2018). Why are RNA virus mutation rates so damn high?. PLoS biology, 16(8), e3000003.
• 4.Stern, A., Te Yeh, M., Zinger, T., Smith, M., Wright, C., Ling, G., … & Andino, R. (2017). The evolutionary pathway to virulence of an RNA virus. Cell, 169(1), 35-46.
• 5.Villarreal, LP, & DeFilippis, VR (2000). A hypothesis for DNA viruses as the origin of eukaryotic replication proteins. Journal of Virology, 74(15), 7079-7084.
• 6. Koonin, EV, & Martin, W. (2005). On the origin of genomes and cells within inorganic compartments. TRENDS in Genetics, 21(12), 647-654.
• 7. Kolakofsky, D. (2015). A short biased history of RNA viruses. RNA, 21(4), 667-669.
• 8.Van Etten, JL, Lane, LC, & Dunigan, DD (2010). DNA viruses: the really big ones (giruses). Annual review of microbiology, 64, 83-99.
• 9.Prangishvili, D., Forterre, P., & Garrett, RA (2006). Viruses of the Archaea: a unifying view. Nature Reviews Microbiology, 4(11), 837-848.
• 10.Canchaya, C., Fournous, G., Chibani-Chennoufi, S., Dillmann, ML, & Brüssow, H. (2003). Phage as agents of lateral gene transfer. Current opinion in microbiology, 6(4), 417-424.

more reference

• 11.Gerstein, M., & Zheng, D. (2006). The real life of pseudogenes. Scientific American, 295(2), 48-55.
• 12. Chuong, EB, Elde, NC, & Feschotte, C. (2017). Regulatory activities of transposable elements: from conflicts to benefits. Nature Reviews Genetics, 18(2), 71.
• 13.Sanmiguel, P., & Bennetzen, JL (1998). Evidence that a recent increase in maize genome size was caused by the massive amplification of intergene retrotransposons. Annals of Botany, 82, 37-44.
• 14.Bell, PJL (2001). Viral eukaryogenesis: was the ancestor of the nucleus a complex DNA virus?. Journal of Molecular Evolution, 53(3), 251-256.
• 15. Huang Yaowei, Li Long, & Yu Lian. (2004). The reverse genetic system of human and animal RNA viruses (Doctoral dissertation).
• 16.Villarreal, LP, & Villareal, LP (1997). On viruses, sex, and motherhood. Journal of Virology, 71(2), 859.
• 17.Dupressoir, A., Lavialle, C., & Heidmann, T. (2012). From ancestral infectious retroviruses to bona fide cellular genes: role of the captured syncytins in placentation. Placenta, 33(9), 663-671.
• 18.La Scola, B., Audic, S., Robert, C., Jungang, L., de Lamballerie, X., Drancourt, M., … & Raoult, D. (2003). A giant virus in amoebae. Science, 299(5615), 2033-2033.
• 19.Xiao, C., Chipman, PR, Battisti, AJ, Bowman, VD, Renesto, P., Raoult, D., & Rossmann, MG (2005). Cryo-electron microscopy of the giant Mimivirus. Journal of molecular biology , 353(3), 493-496.
• 20.Schulz, F., Roux, S., Paez-Espino, D., Jungbluth, S., Walsh, D., Denef, VJ, … & Woyke, T. (2020). Giant virus diversity and host Interactions through global metagenomics. Nature, 1-7.
• 21.Brahim Belhaouari, D., Baudoin, JP, Gnankou, F., Di Pinto, F., Colson, P., Aherfi, S., & La Scola, B. (2019). Evidence of a Cellulosic Layer in Pandoravirus massiliensis Tegument and the Mystery of the Genetic Support of Its Biosynthesis. Frontiers in Microbiology, 10, 2932.
• 22. Forterre, P. (2010). Giant viruses: conflicts in revisiting the virus concept. Intervirology, 53(5), 362-378.
• 23. Shabbir, MZ, Rahman, AU, & Munir, M. (2020). A comprehensive global perspective on phylogenomics and evolutionary dynamics of Small ruminant morbillivirus. Scientific Reports, 10(1), 1-17.