How old is virus




















Tupanvirus has a more complete set of protein-making machinery than any other known virus. This discovery has reignited interest in the theory that viruses arose from complex, free-living cells. Both the theories above assume that cells existed before viruses, and that viruses potentially evolved in the presence of cells.

But there is yet another hypothesis that proposes that viruses existed first, even before cells. In a prehistoric world, viruses might have existed as self-sustaining entities, a sort of ancient machine that could probably reproduce its genetic material. Over time, these prehistoric viruses may have formed complex, organized structures that eventually evolved into cell-like entities. For the time being, these are only theories. The technology and resources we have today cannot confidently test these theories and identify the most plausible explanation for the origin of viruses.

An alternative — yet seemingly impossible — strategy would be to isolate or identify viruses in their primitive forms on other planets such as Mars. Staying on Earth seems like a more plausible approach. Exact numbers are hard to estimate, but the vast majority of animal-to-human spillovers likely result in dead-end infections that never progress past the first individual.

Those factors include how often a virus-carrying animal encounters humans, the means through which a virus is spread, how long a virus can persist outside of a host, and how efficiently a virus can subvert the human immune system. Even factors that seem innocuous—like above-average rainfall, or a local food shortage—can rejigger the dynamics of how humans and animals interact.

This process typically involves a virus latching on to a molecule that studs the outside of a human cell—a bit like a key clicking into a lock. The vast majority of the viruses we encounter simply bounce off our cells, eventually exiting our bodies as harmless visitors.

Sometimes, however, a pathogen manages to slip through. More than viruses are known to cause disease in humans, and all are capable of breaking into human cells. The host molecules that viruses glom on to, which are called receptors, tend to be highly variable from one species to the next, Sawyer says.

Viruses with a lot of genetic flexibility, and particularly those that encode their genomes as RNA rather than DNA, are well-suited to crossing the species divide. Compared to viruses and cells that rely on DNA, RNA viruses tend to be sloppy when copying over their genetic code, introducing mutations at a high rate. This error-prone process creates an immense amount of diversity into populations of RNA viruses , allowing them to adapt to new environments —including new host species—at a rapid pace, says Sarah Zohdy , a disease ecologist at Auburn University.

Neither mutation nor viral interbreeding, however, can guarantee spillover—and viruses that lack one or both traits can still infect a wide range of hosts.

A few years ago, Geoghegan and her colleagues identified a slew of other characteristics common to viruses that cause disease in humans. Their analysis revealed that viruses seemed to benefit from hiding in their hosts for long periods of time without being lethal. Lengthier infections, she says, likely give these stealthy pathogens more time to adapt and spread to new species.

And of course, viruses related to known human pathogens, such as new strains of influenza and the novel coronavirus, are always possible threats. To try to unpick the question of virus evolution, Caetano-Anolles developed a new way to reconstruct the microbial family tree, and retrace bacteria and viruses back to their origins.

But this technique only lets you rewind a million years or so. Caetano-Anolles wanted to go back to the beginnings of life on Earth — around 3. Proteins are high-precision molecular machines — if you change their shape, you disrupt their function. While life can tolerate a continual gentle drift in the genetic code, protein shape is critical and therefore evolves much more slowly. The researchers developed algorithms to compare the protein shapes of 3, viruses and 1, cells.

They found that protein folds were shared between cells and viruses, but 66 folds were unique to viruses. Wherever possible, the team used fossil evidence to put an approximate date on the budding of specific branches.

For example, one particular protein fold was first seen in cyanobacteria blue-green algae , and later appeared in all its descendants. By comparing when cyanobacteria first appeared in the fossil record 2. In fact, his family tree suggests viruses and bacteria share a common ancestor — a fully functioning, self-replicating cell that lived around 3.

The pair hunts for even larger, stranger iterations, which they hope will reveal not only the evolution of giant viruses, but perhaps of all viruses. This story originally appeared in Quanta Magazine , an editorially independent division of SimonsFoundation. All rights reserved. Raw Material for Life Scientists have traditionally thought that viruses were relative latecomers to the evolutionary stage, emerging after the appearance of cells.

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