Viral evolution

Viral evolution is a specialized field within evolutionary biology and virology. It focuses on how viruses change over time to adapt to their environments. Viruses are unique because they often have very short generation times. Many types, specifically RNA viruses, possess high mutation rates. A mutation is a change in the genetic code. In some RNA viruses, there is one or more mutations per genome during every round of replication. While most mutations are useless or even harmful to the virus, natural selection allows beneficial changes to spread. This rapid adaptation helps viruses survive in changing host environments.

The mechanism of viral evolution relies on how viruses replicate. When a virus infects a host, it makes many copies of itself. During this process, errors occur in the genetic material. In host cells, there are tools to fix mistakes in DNA replication. However, these mechanisms do not work for RNA. Consequently, RNA viruses are much more prone to errors. A single virus particle can produce millions of progeny in just one replication cycle. Most of these mutations are "silent," meaning they cause no obvious change. However, some mutations increase a virus's fitness. These changes might help a virus hide from the immune system. They can also make antiviral drugs less effective.

Viruses change through different processes like antigenic drift and genetic shift. Antigenic drift involves the gradual accumulation of mutations in viral genes over time. In contrast, genetic shift occurs when two similar viral strains infect the same cell. These two strains can "shuffle" or swap their genes. This sudden change can result in new and more virulent strains. Different viruses also evolve at different speeds. For example, HIV evolves very rapidly. Other viruses, such as GB virus C, evolve much more slowly. Even within a single virus, different genomic regions may evolve at different rates due to varying selective pressures. This was observed in the SARS-CoV-2 virus during the COVID-19 pandemic.

Scientists use several classical hypotheses to explain how viruses first emerged. The regressive hypothesis suggests viruses were once small cells that lived as parasites. Over time, they lost genes that were not needed for parasitism. The bacteria rickettsia and chlamydia provide support for this idea. The cellular origin hypothesis, or "escape hypothesis," suggests viruses evolved from genetic material that escaped larger organisms. This material could come from plasmids or transposons. Transposons are mobile genetic elements often called "jumping genes." Barbara McClintock discovered these in maize in 1950. The co-evolution hypothesis, or "virus-first hypothesis," proposes that viruses and cells evolved from complex molecules at the same time.

A newer theory called the chimeric-origins hypothesis was proposed in 2019. This model suggests that different parts of a virus have different origins. The replication modules likely came from the primordial genetic pool. However, the structural proteins likely evolved from diverse host proteins. This theory combines features of both the escape and virus-first hypotheses. Some viruses also exist as "satellites" or defective viruses. The hepatitis delta virus is a defective virus with an RNA genome. It requires the hepatitis B virus to provide a protein coat for transmission. Similarly, the sputnik virophage depends on the mimivirus to function.

Because viruses are too small to form traditional fossils, scientists use paleovirology to study their history. They look for endogenous viral elements, known as EVEs. These are remnants of ancient viral genes that invaded a host's germline. Most vertebrate species contain hundreds or thousands of these sequences. These EVEs allow researchers to reconstruct the evolutionary history of viruses. Scientists also use a "molecular clock" to estimate when different viruses diverged. By measuring mutation rates, they can infer dates of divergence from contemporary genomes. This provides a window into the deep past of the virosphere.

Understanding viral evolution is critical for modern medicine and epidemiology. Rapid mutations cause significant challenges in developing vaccines and antiviral drugs. Resistant mutations often appear within weeks or months of starting a treatment. This is especially true for diseases like influenza, AIDS, and hepatitis. One theoretical model used to study this is the quasispecies model. This model defines a viral quasispecies as a group of closely related strains competing in an environment. Studying these patterns helps scientists prepare for emerging viral threats.