How Viruses Evolve

• How do viruses from animals gain the ability to spread in people?
• Where do new viral strains come from?
• Why do we need a new flu vaccine each year?
• Can a virus mutate and become even more dangerous?

Like all living organisms, viruses change over time. In other words, they evolve.

To get to the answers to these questions and more, it’s helpful to dig into some ideas around how viruses evolve. This page explores some of these ideas, including mutation and gene shuffling. These topics can be a little tricky to grasp, especially if your last biology lesson is a distant, foggy memory. But if you want to understand the answers to these questions, keep reading. It’ll be worth the effort.

Are viruses alive? For the answer, visit FAQs About Viruses.

Usually when an animal virus first infects a person, it's inefficient. Viral replication may be very slow. And few new viruses may be released. It may take exposure to larger numbers of viruses to cause an infection. That’s because viral proteins involved in infection, replication, and spread are fine-tuned to their host. When a virus first makes a jump, it is still optimized for the original host’s internal environment.

But with an initial infection in a new host species, a virus has an opportunity to adapt. The main mechanism that drives the adaptation process is mutation.

Most viruses cannot infect humans. To learn more about what has to happen for animal viruses to jump to people, visit When Viruses Jump Hosts.

Mutation lets viruses make gradual adjustments that fine-tune it to its host. The instructions for building viral proteins are found in genes, in the genetic information that sits in the virus’s center. To make more viruses, this genetic information must be copied. A mutation is an error, like a typo, that happens during the copying process. A mutation can change a gene’s instructions so that it codes for a slightly different protein.

Most protein changes make it harder for the virus to spread. But even during a weak infection, viral genetic information is copied millions of times over. By chance, a mutation may cause a change in a protein that makes it more compatible with the new host. For example, it could fit better with a surface receptor on host cells. Or it could work better at the new host’s body temperature.

A virus with a helpful mutation will spread more efficiently from cell to cell. Each newly infected cell copies the virus, making more viruses with the same advantage. And each time the genetic information is copied, there’s an opportunity for another mutation that can further improve the virus’s efficiency. With the right changes, the virus may be able to spread to more human hosts. This means more rounds of replication, and more opportunities for mutations.

Each mutation may cause only a small change to one protein. Yet over time, which can be months or even weeks, a virus can accumulate multiple mutations that together make it spread efficiently through its new host population.

Scientists use host adaptation to their advantage when they develop weakened (or attenuated) vaccines. The attenuated measles vaccine was grown in chicken cells. In later stages, it was also grown at a temperature lower than human body temperature. Over time, the virus mutated to grow better in these conditions. That made it less effective at spreading between people—but it still causes an immune response that protects people from getting measles. This vaccine has been in use since 1968.

To learn more about how vaccines are made, visit Types of Vaccines.

Through gene shuffling, viruses can evolve in even bigger leaps. When two related viruses infect a host at the same time, they can share or reshuffle their genes. They can rearrange their genetic information to make new viral strains that carry genes, or pieces of genes, from both.

One version of gene shuffling, called recombination, has allowed related coronaviruses to share helpful gene variations. This process has contributed to the diversity of coronaviruses and its success in multiple species, including bats, people, and many other mammals.

There is evidence of recombination in SARS-CoV-2, the novel coronavirus that caused the COVID-19 pandemic. SARS-CoV-2 is most similar to a virus from bats—but the part of the virus that binds to a surface receptor on human cells is most similar to a virus from pangolins. This suggests that two different viruses recombined to make a new virus with genetic information from both. That reshuffling event may have made it possible for the virus to then make the jump to people. There’s evidence that this type of gene sharing has happened before, so we should expect it to happen again. A similar receptor-binding protein is found in SARS CoV, the coronavirus that caused the SARS outbreak of 2003.

Influenza A, the virus that causes the flu, reshuffles its genes through a similar process, called reassortment. Influenza is native to water birds, where (like rhinovirus) it has developed into many different strains. It has also spread to other host species, including people, pigs, horses, dogs, and others.

Influenza has a feature that makes it especially easy for it to share its genes. Its 10 (or so) genes are distributed across 8 separate segments. As new virus particles are built, one copy each of all 8 segments are packaged together inside.

Particularly dangerous (for the hosts) is when an individual is infected by influenza viruses from two different species—say a human and a bird strain. Segments from the two strains can be packaged into new viruses in any combination. The result is hybrid viruses that carry a combination of genes from two strains. Through reassortment, a bird strain can gain the ability to infect human cells. An event like this produced the virus that caused the 1918 influenza pandemic.

Together, ongoing mutation and reassortment give influenza a high level of variability. New strains develop each year, often with the ability to evade our immune system. That’s why we need a new flu vaccine every year.

Viruses that combine genes from animal and human strains are especially dangerous. They can be so different from other viruses that circulate in human populations that we have little immune protection against them. Learn more at Why Are Novel Viruses a Big Deal?

New viruses will continue to jump from animals to people—it’s just a matter of which ones and when. And the viruses we’ve been living with will continue to evolve new ways to evade our defenses. But this does not mean we are doomed. There are ways to fight back, and everyone has a role to play.

The most important thing you can do is keep viruses from spreading. If we can limit a virus’s spread, we also limit its ability to develop new mutations that make it resist drugs, vaccines, and other tools for controlling outbreaks.

There’s also evidence that when spread slows, viruses evolve to be less deadly. When a virus can spread easily from person to person, the fastest-replicating viruses spread the farthest. Viruses acquire mutations that make them replicate even faster. This is usually very bad for the host because a fast-replicating virus can overwhelm their immune system. But this evolution toward speed is held in balance by an opposing force: When a virus kills its host too quickly, before it can spread, it reaches a dead end. In an environment where it’s harder for a virus to spread between hosts, a slow-replicating virus is more likely to spread. The virus may acquire mutations that slow its replication speed. This can give the immune system a chance to eliminate the virus. It also buys time for using other measures, like medications and other treatments.

When you use measures like hand washing, distancing, mask wearing, and (when available) vaccines, you can slow a virus’s spread even further—potentially pushing it to evolve to be less deadly.