The recent outbreak of monkeypox virus has called into question the ability of these large DNA viruses to evolve, adapt and change their biology.
Compared to small RNA viruses such as the coronavirus, monkeypox virus and other large DNA viruses are thought to evolve slowly. However, there is clear evidence that this is not really an obstacle for these viruses. In fact, they can adapt to new environments like us.
Although most infections remain mild, smallpox can be a serious, life-threatening illness, resulting in sepsis, encephalitis (inflammation of the brain), and blindness. The most common symptoms are rashes and skin lesions, along with flu-like symptoms and swollen lymph nodes.
Cumulative smallpox cases in the current outbreak
The Monkeypox virus naturally infects wild rodents such as squirrels and mice in West and Central Africa – but it can transfer species to humans and other animals. However, once it jumped to humans, transmission cannot continue and eventually the outbreaks disappear. This is likely because monkeypox has not adapted to its new environment of humans, as infected humans are unlikely to return to wild rodents.
Monkeypox is closely related to the viruses that caused smallpox (smallpox virus) and the virus we used to vaccinate and eradicate smallpox (vaccinia virus). This group of viruses, known as poxviruses, is a kind of large DNA virus, which means that its genome is made up of a chemical known as DNA, like our genome. (Coronavirus and related viruses use a cousin molecule called RNA.)
Other DNA viruses are the large DNA viruses, adenoviruses and herpesviruses, but also small ones such as papillomaviruses and parvoviruses. Viral genomes composed of DNA or RNA are essentially the instructions for creating new viruses, infecting us and causing disease. Changes in instructions can change the biology of the virus.
As we’ve seen with SARS-CoV-2 and its variants, viruses can change the way they behave with respect to spread, disease severity, and vaccine sensitivity. This is due to the accumulated changes in the virus genome. Virus replication generates diversity in its genome, which can be influenced by evolutionary forces such as natural selection to increase frequency and perhaps even outpace older versions.
Evolutionary changes can occur when the virus encounters a new environment to which it is not fully adapted. While all viruses can evolve rapidly due to their vast population sizes and fast generation times, RNA viruses are believed to be masters of evolution because they have high mutation rates due to their small size, and many generally lack the ability to error correction, which means more mutations occur. each time they replicate.
Poxviruses have some characteristics that make them more generalist, including stable infectious particles, giving them more chances to infect. They use very common molecules in your cells to enter and infect, unlike SARS-CoV-2, which needs the specific ACE2 protein to enter our cells.
Large DNA viruses such as monkeypox also contain many genes that target and manipulate different parts of the immune system.
Room for improvement
However, there is clear evidence that improvements can be made because, in humans, transmission of smallpox from monkeys is relatively inefficient, with long incubation periods.
In general, large DNA viruses such as monkeypox are no different from other viruses, and their mutability is the basis for our ability to track and trace outbreaks of monkeypox. They make mistakes and accumulate mistakes, which can be used as fuel for evolution and biological change. There is even evidence from the recent monkeypox outbreak that the host cell is directly mutating the virus genome.
Studies focusing on related poxviruses such as the vaccinia virus have discovered new tricks they can use, which include rapidly amplifying the number of genes they use to attack our immune systems. They can even borrow some of our own genes to help them infect us.
We cannot predict the trajectory that the evolution of apepox will take, so we must take seriously the threat of this virus adapting to its new (human) hosts. And we need to use every public health tool at our disposal to stop the current outbreak in all countries – including those where it is endemic.
This article is republished from The Conversation under a Creative Commons license. Read the original article.
Connor Bamford receives funding from UKRI, Wellcome Trust, British Medical Association Foundation, SFI.