Viruses evolve

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 To learn more about how vaccines are made, visit Types of Vaccines. It's happening all the time. Rhinovirus, a cause of the common cold, is a good example.

Rhinoviruses did not recently jump from animals; they have specialized in human hosts for thousands of years, if not longer. And they can spread easily through a population.

People who are infected get better after a few days. Before long, there are few non-immune people left for the virus to infect. But rhinovirus can evolve. With thousands of people infected, each shedding billions of virus particles, chances are good that a helpful mutation will come along. If the change makes a single virus particle resist the defenses of a previously infected host, the virus can then multiply and spread. This is how new strains arise. And they can easily develop within a single cold season.

Rhinovirus has gone through changes like this many times over. Today there are at least forms of rhinovirus circulating among us, each of which produces a distinct immune response.

HIV can evolve within an individual host. Each time the immune system learns to recognize the virus, a new copy comes along with a chance mutation that allows it to escape detection. This process also allows HIV to evolve resistance to antiviral drugs. To gain resistance, a single virus particle would need to develop multiple helpful mutations at once—and the chances of that happening are exceedingly low.

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. 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. Recombination happens in viruses with one continuous strand of genetic information. The resulting hybrid viruses have pieces of genetic information from two different viruses. Recombination is common in coronaviruses, and it can lead to new viral strains.

Reassortment happens in viruses with segmented genomes. Segments of genetic information from two strains can be shuffled together in new combinations. 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.

Although high error rates, variation, and quasispecies generation can be seen in laboratory settings, natural isolates, such as lyssaviruses and measles virus, tend to be relatively homogeneous.

Lyssavirus persistent infections in natural host might contribute to this stability. However, measles virus is a strictly human-specific acute infection so its stability is likely due to purifying selection.

Large DNA viruses of bacteria, archaea, and eukaryotes appear to be evolutionarily linked. Although little sequence conservation can be identified between the T4 phage of bacteria, the halophage of archaea, the members of the family Phycodnaviridae infecting algae, and the herpes viruses of vertebrate eukaryotes, all show similarities in their gene programs, DNA polymerase types, capsid structures, and capsid assembly, consistent with a common ancestor.

The bacterial DNA viruses would appear to represent the ancestor of all these viruses, but the origins of these phages now appear lost in the primordial gene pool. These DNA viruses can have large genomes that could not be sustained by error-prone replication. Giant bacterial phage genomes Bacillus megaterium phage G, of about genes , and algal phycodnaviruses have now been characterized. Even larger DNA viruses of amoeba acanthamoeba polyphaga mimivirus coding for more than genes are known to be abundant in some water habitats.

This corresponds to about 10 24 productive infections per second on a global scale. Most host-restricted phage lineages clearly conserve sets of core proteins especially capsid genes , but others the broader T-even phages do not conserve any hallmark genes.

Hallmark genes, when present, are usually recognized by conserved domains within proteins, such as replication and structural proteins. Replicator strategy and gene order are also frequently conserved. Phage also tends to conserve genes that are active against other phage i. With the sequencing of numerous phage genomes, however, a large number of novel genes have been identified.

Currently, full genomes of tailed phage and prophage from bacterial genomes have been sequenced. Comparative genomics, especially of lactobacterial phages, suggest that most phage genomes evolve as mosaics, with sharp boundaries between genes as well as at protein domains within genes see Figure 5. Recombination between lytic, temperate, and cryptic prophages appears to account for this gene and subgene domain variation.

Some specific phages have mechanisms to generate specific gene diversity such as bordetella phage using RT for surface receptor diversity , but most diversity is the product of recombination. Two broad patterns of phage variation have been observed corresponding to host-unassociated lytic and host-associated congruent temperate phage. The general picture for tailed phage of bacteria is that they are not the products of reduction of host genomes.

Genome comparison of temperate S. Probable gene functions are indicated and genomes have been divided into functional units. Genes belonging to the same module are indicated with the same color. Areas of shading indicate regions of major difference. Antonie van Leeuwenhoek 73— As noted, evolutionary links between tailed phage and large DNA viruses of eukaryotes are apparent. Thus, phycodnaviruses show hybrid characteristics of prokaryotic and eukaryotic viruses. These exist in distinct classes that are typically specific for each viral lineage and are usually the most highly conserved of the set of core genes within a viral lineage.

However, some viruses, such as the white spot syndrome virus WSSV infecting shrimps, have almost no genes in common with other DNA viruses. Generally, the specific set of core genes is clade specific. The first fully sequenced viral genome tree was that of the baculoviruses see Figure 6. The overall pattern of evolution shows the conservation of the core set in which most clades can be differentiated from one another mainly by acquisition of several novel viral genes although some lineage-specific gene loss is also apparent.

In another example, coccolithoviruses differ from related phycodnaviruses by the acquisition of kbp gene set, including six subunits of DdDp core genes. Similar patterns of divergence can be seen with the herpesvirus family members. In addition, most herpesvirus clades also show coevolution with their host. However, the poxviruses orthopoxviruses , show a different overall evolutionary pattern and are not congruent with host. The more ancestral orthopoxvirus members, such as cowpox virus and mousepox virus, have greater gene numbers that appear to have been lost in the human-specific and virulent smallpox virus.

Avipoxviruses have even greater gene diversity but the entomopoxviruses are the most complex and diverse of all. The complexity and brick shape of the poxviruses originally inspired the view that these viruses might evolve from bacterial cells following the reduction of complexity. However, DNA sequencing makes it clear that viral core genes have no bacterial analogs.

In some instances, viral lineages have clearly fused with other viral and host lineages. The polydnaviruses circular DNA viruses are fused into their host genomes as endogenous DNA viruses of some parasitoid wasps, essential for survival of the wasp larvae.

Gene content map of 13 complete sequences of baculoviruses, including the genus Granulovirus. The tree shows the most parsimonious hypothesis of changes in gene content during baculovirus evolution. Colors and shapes indicate gene conservation, acquisition, and loss.

Annual Review of Entomology —, with permission from Annual Reviews. The small, double-stranded, circular DNA viruses Papillomaviridae and Polyomaviridae show evolutionary patterns that are highly host linked. Virus and host evolution are mostly congruent, and virus evolution tends to be slow. For example, approximately human papillomaviruses show congruent evolution with human and primate host. This seems to be due to both a highly species- and tissue-specific virus replication, as well as a tendency to establish persistent infections.

However, the rolling circular replicon RCR viruses, such as parvoviruses, can have distinct evolution patterns. Such rates are at the lower end of those seen with RNA viruses. Other poorly characterized small eukaryotic DNA viruses, such as human torque teno virus, are asymptomatic but show high variation during persistence for unknown reasons. Retroviruses present a special problem in understanding patterns of eukaryotic virus evolution.

Like prophage of bacteria, retroviruses both stably colonize their host as endogenous or genomic retroviruses ERVs that are often defective, but may also sometimes emerge from their host especially rodents to produce autonomous virus. In addition, retroviruses are polyphyletic and prone to generating quasispecies due to high error rates as well as high rates of recombination.

The most common conserved retrovirus genome elements are domains within the long terminal repeats LTRs , RT, integrase, protease, gag protein, and env protein. Of these, env are the most often altered or deleted in host genomes. However, each of these retroviral elements can potentially have distinct patterns of evolution and conservation, generating distinct dendrograms. Vertebrates, especially mammals, seem to host many retroviral elements within their genomes.

Their autonomous retroviruses have a tendency to infect cells of the immune system. Murine leukemia virus MLV is the best-studied simple autonomous retrovirus, but many endogenous MLV relatives also exist. Retroviruses are present in genomes of early eukaryotes but significantly expanded in vertebrates.

Gypsy-like retroviruses aka chromoviruses, defined via RT and gag similarity are often found conserved as full-length elements including env genes in most lower eukaryote genomes e.

Many endogenous retroviruses are congruent with host evolution, whereas other ERVs are recently acquired and highly host specific. In terms of gene diversity, the retroviral env are the most diverse. There are five RT-based families recognized such as Retroviridae, Hepadnaviridae, Caulimovoridae, Pseudoviridae, and Metaviridae , the latter three being especially prevalent as genomic elements in flowering plants especially Gypsy. Yet not all retroviruses seem able to colonize host germ line.

For example, lentiviruses such as simian immunodeficiency virus SIV and HIV show no examples of endogenization compared to the simpler MLV-related viruses that can be both autonomous i. These non-LTR elements, have distinct nonretroviral mechanistic features and core protein domains, but retain some virus-like domains of RT; thus, they appeared to predate retroviruses. However, we now know that gypsy-like retroviruses were present in the earliest eukaryotes.

In addition, some LTR-containing elements, such as Gypsy, had initially been considered ancestral to retroviruses because all copies seemed to be defective. However, it is now established that complete gypsy retroviruses are conserved as ERVs in some yeast and Drosophila strains.

Thus, although endogenous and exogenous retroviruses appear to evolve from each other, there is no evidence that exogenous retroviruses have emerged from non-LTR LINE-like elements. The congruence between ERVs and host eukaryote evolution is sometimes striking. Clearly, retrovirus evolution is highly intertwined with that of their hosts. A remaining concern of virus evolution is to understand the emergence of new viral pathogens. The unpredictable and stochastic nature of such virulent adaptations makes predictions difficult, as the link between virulence and evolution is vague.

For example, the genetic changes that made the SARS virus persisting in bats into an acute human pathogen are still not predictable. Viral fitness and selection, and how they change from persistent states with acute species jumps, are not yet defined. However, some variables contribute to the likelihood of viral emergence, such as virus ecology. The population density and dynamics of the new host and the ecological interactions between new and stable viral host are often crucial.

The emergence of HIV-1 from different, persistent SIVs of African monkeys through chimpanzees into a new human disease, for example, includes the same issues.

Also, the potential emergence of pandemic human influenza from avian Anatiformes sources, such as H5N1, remains a great concern. Thus, virus evolution will continue to interest us as we seek to predict, control, or eradicate viral agents of disease. National Center for Biotechnology Information , U. Encyclopedia of Virology. Published online Jul Guest Editor s : Brian W. Guest Editor s : Marc H. Author information Copyright and License information Disclaimer.

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Abstract The study of virus evolution has historically been concerned with disease and its emergence and has not been integrated into the general study of evolution. Introduction The initial study of virus evolution sought to explain how virus variation affects viral and host survival and to understand viral disease.

Open in a separate window. Figure 1. Figure 2. Virus Evolution as a Basic Science Virus variation is a global issue. Distinctions from Host Evolution For the most part, virus evolution conforms to the same Darwinian principles as host evolution, involving variation and natural selection. A History of Virus Evolution The coherent study of virus evolution awaited the development of sequence technology to measure mutations and genetic variation in viral populations.

Error-Prone Replication and Quasispecies In the s, Manfred Eigen and also Peter Shuster developed a fundamental theoretical model of virus evolution.

Error Catastrophe, Sequence Space Quasispecies theory also predicts a situation known as error catastrophe, defined as an error rate threshold at which information is lost and the system decays.

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