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21.1B: Evolution of Viruses - Biology

21.1B: Evolution of Viruses - Biology


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The evolution of viruses is speculative as they do not fossilize; biochemical and genetic information is used to create virus histories.

Learning Objectives

  • Describe the difficulties in determining the origin of viruses

Key Points

  • Scientists agree that viruses don’t have a single common ancestor, but have yet to agree on a single hypothesis about virus origins.
  • The devolution or the regressive hypothesis suggests that viruses evolved from free-living cells.
  • The escapist or the progressive hypothesis suggests that viruses originated from RNA and DNA molecules that escaped from a host cell.
  • The self-replicating hypothesis posits a system of self-replication that most probably involves evolution alongside the host cells.

Key Terms

  • self-replicating: able to generate a copy of itself
  • devolution: degeneration (as opposed to evolution)

Evolution of Viruses

Although biologists have accumulated a significant amount of knowledge about how present-day viruses evolve, much less is known about how viruses originated in the first place. When exploring the evolutionary history of most organisms, scientists can look at fossil records and similar historic evidence. However, viruses do not fossilize, so researchers must conjecture by investigating how today’s viruses evolve and by using biochemical and genetic information to create speculative virus histories.

While most findings agree that viruses don’t have a single common ancestor, scholars have yet to find one hypothesis about virus origins that is fully accepted in the field. One possible hypothesis, called devolution or the regressive hypothesis, proposes to explain the origin of viruses by suggesting that viruses evolved from free-living cells. However, many components of how this process might have occurred are a mystery. A second hypothesis (called escapist or the progressive hypothesis) accounts for viruses having either an RNA or a DNA genome and suggests that viruses originated from RNA and DNA molecules that escaped from a host cell. A third hypothesis posits a system of self-replication similar to that of other self-replicating molecules, probably evolving alongside the cells they rely on as hosts; studies of some plant pathogens support this hypothesis.

As technology advances, scientists may develop and refine further hypotheses to explain the origin of viruses. The emerging field called virus molecular systematics attempts to do just that through comparisons of sequenced genetic material. These researchers hope to one day better understand the origin of viruses, a discovery that could lead to advances in the treatments for the ailments they produce.


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Scientists uncover the mysteries of how viruses evolve

IMAGE: In a directed evolution experiment, a protein shell naturally occurring in bacteria evolved into a protein container that can encapsulate RNA, mimicking a genome packaging mechanism the team previously discovered. view more

Credit: ETH Zürich / Stephan Tette

The team say their findings have implications for the treatment of viruses in future.

Researchers from the Universities of York and Leeds, collaborating with the Hilvert Laboratory at the ETH Zürich, studied the structure, assembly and evolution of a 'container' composed of a bacterial enzyme.

The study - published in the journal Science - details the structural transformation of these virus-like particles into larger protein 'containers'.

It also reveals that packaging of the genetic cargo in these containers becomes more efficient during the later stages of evolution. They show that this is because the genome inside evolves hallmarks of a mechanism widely used by natural viruses, including Covid-19, to regulate their assembly. That mechanism was a joint discovery of the York and Leeds team. Professor Reidun Twarock, from the University of York's Departments of Mathematics and Biology, and the York Cross-disciplinary Centre for Systems Analysis, said: "Using a novel interdisciplinary technique developed in our Wellcome Trust funded team in Leeds and York, we were able to demonstrate that this artificial system evolved the molecular hallmarks of a 'virus assembly mechanism', enabling efficient packaging of its genetic cargo."

In its evolution, the artificial virus-like particle efficiently packages and protects multiple copies of its own encoding messenger RNA.

Professor Peter Stockley from the University of Leeds' Astbury Centre for Structural Molecular Biology, said "What's remarkable is this artificial virus-like particle evolves to be more efficient in packaging RNA. Our collaboration shows that following the evolutionary steps the encapsidated messenger RNAs incorporate more Packaging Signals than the starting RNAs. In other words, the phenomenon we have been working on in natural viruses "evolves" in an artificial particle, and the results in this paper therefore describe a process that may have occurred in the early evolution of viruses. This understanding enables us to exploit these containers as delivery vehicles for gene therapeutic purposes."

Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.


21.1 Viral Evolution, Morphology, and Classification

In this section, you will explore the following questions:

  • How were viruses first discovered and how are they detected?
  • What three hypotheses describe the evolution of viruses?
  • What is the basic structure of a virus?
  • How are viruses classified?

Connection for AP ® Courses

The first organisms that originated about 3.5 billion years ago were prokaryotes that possessed the structures and metabolic processes associated with cells (refer to the Cell Structure chapter). As discussed in the chapter on cell structure, prokaryotic cells are much smaller than eukaryotic cells and inhabit just about every square inch of our planet, from the most inhospitable environments to the surface of the skin. Viruses are much smaller than prokaryotes and much simpler in structure. They must reproduce inside a host cell. Their origin is still a mystery to us, but we do know that they can make us very sick.

Viruses have a basic structure: a DNA or RNA core surrounded by an outer capsid of proteins. Some viruses have an outer phospholipid envelope. As we will explore in more detail, many viruses use some sort of glycoprotein to attach to their host cells. Viruses infect all known cell types and use the host cell’s replication proteins and metabolic machinery to replicate. Classification of viruses is challenging, but one method categorizes them based on how they produce their mRNA. Retroviruses (also called RNA viruses) use the enzyme reverse transcriptase to transcribe DNA from RNA. (In the Genes and Proteins chapter we learned that the usual flow of genetic information is from DNA to RNA to protein.) Common viruses include bacteriophage T4, adenovirus, and HIV retrovirus.

Information presented and the examples highlighted in the section support concepts outlined in Big Idea 3 of the AP ® Biology Curriculum Framework. The AP ® Learning Objectives listed in the Curriculum Framework provide a transparent foundation for the AP ® Biology course, an inquiry-based laboratory experience, instructional activities, and AP ® exam questions. A learning objective merges required content with one or more of the seven science practices.

Big Idea 3 Living systems store, retrieve, transmit and respond to information essential to life processes.
Enduring Understanding 3.A Heritable information provides for continuity of life.
Essential Knowledge 3.A.1 DNA, and in some cases RNA, is the primary source of heritable information.
Science Practice 6.5 The student can evaluate alternative scientific explanations.
Learning Objective 3.1 The student is able to construct scientific explanations that use the structures and mechanisms of DNA and RNA to support the claim that DNA and, in some cases, that RNA are the primary sources of heritable information.

The Science Practice Challenge Questions contain additional test questions for this section that will help you prepare for the AP exam. These questions address the following standards:
[APLO 2.20][APLO 3.3][APLO 3.29][APLO 3.30][APLO 2.22][APLO 2.26][APLO 1.31][APLO 1.27][APLO 1.30]

Discovery and Detection

Viruses were first discovered after the development of a porcelain filter, called the Chamberland-Pasteur filter, which could remove all bacteria visible in the microscope from any liquid sample. In 1886, Adolph Meyer demonstrated that a disease of tobacco plants, tobacco mosaic disease, could be transferred from a diseased plant to a healthy one via liquid plant extracts. In 1892, Dmitri Ivanowski showed that this disease could be transmitted in this way even after the Chamberland-Pasteur filter had removed all viable bacteria from the extract. Still, it was many years before it was proven that these “filterable” infectious agents were not simply very small bacteria but were a new type of very small, disease-causing particle.

Virions, single virus particles, are very small, about 20–250 nanometers in diameter. These individual virus particles are the infectious form of a virus outside the host cell. Unlike bacteria (which are about 100-times larger), we cannot see viruses with a light microscope, with the exception of some large virions of the poxvirus family. It was not until the development of the electron microscope in the late 1930s that scientists got their first good view of the structure of the tobacco mosaic virus (TMV) (Figure 21.1) and other viruses (Figure 21.2). The surface structure of virions can be observed by both scanning and transmission electron microscopy, whereas the internal structures of the virus can only be observed in images from a transmission electron microscope. The use of these technologies has allowed for the discovery of many viruses of all types of living organisms. They were initially grouped by shared morphology. Later, groups of viruses were classified by the type of nucleic acid they contained, DNA or RNA, and whether their nucleic acid was single- or double-stranded. More recently, molecular analysis of viral replicative cycles has further refined their classification.

Evolution of Viruses

Although biologists have accumulated a significant amount of knowledge about how present-day viruses evolve, much less is known about how viruses originated in the first place. When exploring the evolutionary history of most organisms, scientists can look at fossil records and similar historic evidence. However, viruses do not fossilize, so researchers must conjecture by investigating how today’s viruses evolve and by using biochemical and genetic information to create speculative virus histories.

While most findings agree that viruses don’t have a single common ancestor, scholars have yet to find a single hypothesis about virus origins that is fully accepted in the field. One such hypothesis, called devolution or the regressive hypothesis, proposes to explain the origin of viruses by suggesting that viruses evolved from free-living cells. However, many components of how this process might have occurred are a mystery. A second hypothesis (called escapist or the progressive hypothesis) accounts for viruses having either an RNA or a DNA genome and suggests that viruses originated from RNA and DNA molecules that escaped from a host cell. A third hypothesis posits a system of self-replication similar to that of other self-replicating molecules, likely evolving alongside the cells they rely on as hosts studies of some plant pathogens support this hypothesis.

As technology advances, scientists may develop and refine further hypotheses to explain the origin of viruses. The emerging field called virus molecular systematics attempts to do just that through comparisons of sequenced genetic material. These researchers hope to one day better understand the origin of viruses, a discovery that could lead to advances in the treatments for the ailments they produce.

Viral Morphology

Viruses are acellular, meaning they are biological entities that do not have a cellular structure. They therefore lack most of the components of cells, such as organelles, ribosomes, and the plasma membrane. A virion consists of a nucleic acid core, an outer protein coating or capsid, and sometimes an outer envelope made of protein and phospholipid membranes derived from the host cell. Viruses may also contain additional proteins, such as enzymes. The most obvious difference between members of viral families is their morphology, which is quite diverse. An interesting feature of viral complexity is that the complexity of the host does not correlate with the complexity of the virion. Some of the most complex virion structures are observed in bacteriophages, viruses that infect the simplest living organisms, bacteria.

Morphology

Viruses come in many shapes and sizes, but these are consistent and distinct for each viral family. All virions have a nucleic acid genome covered by a protective layer of proteins, called a capsid. The capsid is made up of protein subunits called capsomeres. Some viral capsids are simple polyhedral “spheres,” whereas others are quite complex in structure.

In general, the shapes of viruses are classified into four groups: filamentous, isometric (or icosahedral), enveloped, and head and tail. Filamentous viruses are long and cylindrical. Many plant viruses are filamentous, including TMV. Isometric viruses have shapes that are roughly spherical, such as poliovirus or herpesviruses. Enveloped viruses have membranes surrounding capsids. Animal viruses, such as HIV, are frequently enveloped. Head and tail viruses infect bacteria and have a head that is similar to icosahedral viruses and a tail shape like filamentous viruses.

Many viruses use some sort of glycoprotein to attach to their host cells via molecules on the cell called viral receptors (Figure 21.3). For these viruses, attachment is a requirement for later penetration of the cell membrane, so they can complete their replication inside the cell. The receptors that viruses use are molecules that are normally found on cell surfaces and have their own physiological functions. Viruses have simply evolved to make use of these molecules for their own replication. For example, HIV uses the CD4 molecule on T lymphocytes as one of its receptors. CD4 is a type of molecule called a cell adhesion molecule, which functions to keep different types of immune cells in close proximity to each other during the generation of a T lymphocyte immune response.

Among the most complex virions known, the T4 bacteriophage, which infects the Escherichia coli bacterium, has a tail structure that the virus uses to attach to host cells and a head structure that houses its DNA.

Adenovirus, a non-enveloped animal virus that causes respiratory illnesses in humans, uses glycoprotein spikes protruding from its capsomeres to attach to host cells. Non-enveloped viruses also include those that cause polio (poliovirus), plantar warts (papillomavirus), and hepatitis A (hepatitis A virus).

Enveloped virions like HIV, the causative agent in AIDS, consist of nucleic acid (RNA in the case of HIV) and capsid proteins surrounded by a phospholipid bilayer envelope and its associated proteins. Glycoproteins embedded in the viral envelope are used to attach to host cells. Other envelope proteins are the matrix proteins that stabilize the envelope and often play a role in the assembly of progeny virions. Chicken pox, influenza, and mumps are examples of diseases caused by viruses with envelopes. Because of the fragility of the envelope, non-enveloped viruses are more resistant to changes in temperature, pH, and some disinfectants than enveloped viruses.

Overall, the shape of the virion and the presence or absence of an envelope tell us little about what disease the virus may cause or what species it might infect, but they are still useful means to begin viral classification (Figure 21.4).


Viruses play critical role in evolution and survival of the species

This illustration shows the four stages of mouse spermatogenesis analyzed in research published Sept. 7, 2020, in Nature Structural & Molecular Biology. Credit: Cincinnati Children's

As the world scrambles to control the growing COVID-19 coronavirus pandemic, new research in Nature Structural & Molecular Biology shows viruses also play a key evolutionary role in mammals' ability to reproduce and survive.

Scientists in the Cincinnati Children's Perinatal Institute and at Azabu University in Japan obtained their data by studying laboratory mice and human germline cells.

In two separate papers appearing in the same edition of the journal, they reveal two distinct and fundamental processes underlying germline transcriptomes. They also show that species-specific transcriptomes are fine-tuned by endogenous retroviruses in the mammalian germline

Germline transcriptomes include all the messenger RNA in germline cells, which contain either the male or female half of chromosomes passed on as inherited genetic material to offspring when species mate. This means that germline transcriptomes define the unique character of sperm and egg to prepare for the next generation of life.

Although the studies are separate they complement one another, according to Satoshi Namekawa, Ph.D., principal investigator on both papers and a scientist in the Division of Reproductive Science at Cincinnati Children's.

"One paper, Maezawa and Sakashita et al., explores super-enhancers, which are robust and evolutionally conserved gene regulatory elements in the genome. They fuel a tightly regulated burst of essential germline genes as sperm start to form," Namekawa said.

"The second study, Sakashita et al., involves endogenous retroviruses that act as another type of enhancer—gene regulatory elements in the genome—to drive expression of newly evolved genes. This helps fine tune species-specific transcriptomes in mammals like humans, mice, and so on.

Together the studies have significant potential ramifications for clinical practice, according to study authors, who include a multi-disciplinary mix of developmental biologists, bioinformaticians and immuno-biologists. Dysregulation of gene expression in the formation of male sperm is closely associated with male infertility and birth defects.

Viruses, especially endogenous retroviruses (ERVs) that are an inherent part of mammalian biology, can dramatically influence gene expression, investigators report. ERVs are molecular remnants of retroviruses that infect the body and over time incorporate into the genome.

"What we learn from our study is that, in general, viruses have major roles in driving evolution," Namekawa explained. "In the long-term, viruses have positive impacts to our genome and shape evolution."

The study, Maezawa and Sakashita et al., combined biological testing of mouse models and human germline cells with computational biology, including genome-wide profiling of gene regulatory elements in germline cells.

Those tests revealed that the the genome-wide reorganization of super-enhancers drives bursts of germline gene expression after germ cells enter meiosis, a specialized form of cell division that produces the haploid genome of germ cells.

The study further demonstrates the molecular process through whichsuper-enhancer switching takes place in germ cells. Super-enhancers are regulated by two molecules that act as gene-burst control switches—the transcription factor A-MYB and SCML2, a critical silencing protein in sperm formation.

TEs and Jumping Genes

Endogenous retroviruses are a group of transposable elements (TEs), mobile genetic elements that account for approximately 40-50 percent of a given mammalian genome. Also referred to as "jumping genes," TEs have long been considered genetic threats because transposition can be harmful if, for example, the process disrupts protein-coding genes.

Building on findings from the 1950s that TEs can function as genetic regulatory elements, Namekawa and his collaborators (Sakashita et al.) produced data showing that ERV-driven mechanisms help fine tune species-specific transcriptomes.


Evolutionary origins of human herpes simplex viruses 1 and 2

Herpesviruses have been infecting and codiverging with their vertebrate hosts for hundreds of millions of years. The primate simplex viruses exemplify this pattern of virus-host codivergence, at a minimum, as far back as the most recent common ancestor of New World monkeys, Old World monkeys, and apes. Humans are the only primate species known to be infected with two distinct herpes simplex viruses: HSV-1 and HSV-2. Human herpes simplex viruses are ubiquitous, with over two-thirds of the human population infected by at least one virus. Here, we investigated whether the additional human simplex virus is the result of ancient viral lineage duplication or cross-species transmission. We found that standard phylogenetic models of nucleotide substitution are inadequate for distinguishing among these competing hypotheses the extent of synonymous substitutions causes a substantial underestimation of the lengths of some of the branches in the phylogeny, consistent with observations in other viruses (e.g., avian influenza, Ebola, and coronaviruses). To more accurately estimate ancient viral divergence times, we applied a branch-site random effects likelihood model of molecular evolution that allows the strength of natural selection to vary across both the viral phylogeny and the gene alignment. This selection-informed model favored a scenario in which HSV-1 is the result of ancient codivergence and HSV-2 arose from a cross-species transmission event from the ancestor of modern chimpanzees to an extinct Homo precursor of modern humans, around 1.6 Ma. These results provide a new framework for understanding human herpes simplex virus evolution and demonstrate the importance of using selection-informed models of sequence evolution when investigating viral origin hypotheses.

Keywords: co-divergence cross-species transmission homo molecular clock selection zoonosis.


21.1 Viral Evolution, Morphology, and Classification

By the end of this section, you will be able to do the following:

  • Describe how viruses were first discovered and how they are detected
  • Discuss three hypotheses about how viruses evolved
  • Describe the general structure of a virus
  • Recognize the basic shapes of viruses
  • Understand past and emerging classification systems for viruses
  • Describe the basis for the Baltimore classification system

Viruses are diverse entities: They vary in structure, methods of replication, and the hosts they infect. Nearly all forms of life—from prokaryotic bacteria and archaeans, to eukaryotes such as plants, animals, and fungi—have viruses that infect them. While most biological diversity can be understood through evolutionary history (such as how species have adapted to changing environmental conditions and how different species are related to one another through common descent), much about virus origins and evolution remains unknown.

Discovery and Detection

Viruses were first discovered after the development of a porcelain filter—the Chamberland-Pasteur filter—that could remove all bacteria visible in the microscope from any liquid sample. In 1886, Adolph Meyer demonstrated that a disease of tobacco plants— tobacco mosaic disease —could be transferred from a diseased plant to a healthy one via liquid plant extracts. In 1892, Dmitri Ivanowski showed that this disease could be transmitted in this way even after the Chamberland-Pasteur filter had removed all viable bacteria from the extract. Still, it was many years before it was proved that these “filterable” infectious agents were not simply very small bacteria but were a new type of very small, disease-causing particle.

Most virions , or single virus particles, are very small, about 20 to 250 nanometers in diameter. However, some recently discovered viruses from amoebae range up to 1000 nm in diameter. With the exception of large virions, like the poxvirus and other large DNA viruses, viruses cannot be seen with a light microscope. It was not until the development of the electron microscope in the late 1930s that scientists got their first good view of the structure of the tobacco mosaic virus (TMV) (Figure 21.1), discussed above, and other viruses (Figure 21.2). The surface structure of virions can be observed by both scanning and transmission electron microscopy, whereas the internal structures of the virus can only be observed in images from a transmission electron microscope. The use of electron microscopy and other technologies has allowed for the discovery of many viruses of all types of living organisms.

Evolution of Viruses

Although biologists have a significant amount of knowledge about how present-day viruses mutate and adapt, much less is known about how viruses originated in the first place. When exploring the evolutionary history of most organisms, scientists can look at fossil records and similar historic evidence. However, viruses do not fossilize, as far as we know, so researchers must extrapolate from investigations of how today’s viruses evolve and by using biochemical and genetic information to create speculative virus histories.

Most scholars agree that viruses don’t have a single common ancestor, nor is there a single reasonable hypothesis about virus origins. There are current evolutionary scenarios that may explain the origin of viruses. One such hypothesis, the “devolution” or the regressive hypothesis, suggests that viruses evolved from free-living cells, or from intracellular prokaryotic parasites. However, many components of how this process might have occurred remain a mystery. A second hypothesis, the escapist or the progressive hypothesis, suggests that viruses originated from RNA and DNA molecules, or self-replicating entities similar to transposons or other mobile genetic elements, that escaped from a host cell with the ability to enter another. A third hypothesis, the virus first hypothesis, suggests that viruses may have been the first self-replicating entities before the first cells. In all cases, viruses are probably continuing to evolve along with the cells on which they rely on as hosts.

As technology advances, scientists may develop and refine additional hypotheses to explain the origins of viruses. The emerging field called virus molecular systematics attempts to do just that through comparisons of sequenced genetic material. These researchers hope one day to better understand the origin of viruses—a discovery that could lead to advances in the treatments for the ailments they produce.

Viral Morphology

Viruses are noncellular , meaning they are biological entities that do not have a cellular structure. They therefore lack most of the components of cells, such as organelles, ribosomes, and the plasma membrane. A virion consists of a nucleic acid core, an outer protein coating or capsid , and sometimes an outer envelope made of protein and phospholipid membranes derived from the host cell. Viruses may also contain additional proteins, such as enzymes, within the capsid or attached to the viral genome. The most obvious difference between members of different viral families is the variation in their morphology, which is quite diverse. An interesting feature of viral complexity is that the complexity of the host does not necessarily correlate with the complexity of the virion. In fact, some of the most complex virion structures are found in the bacteriophages —viruses that infect the simplest living organisms, bacteria.

Morphology

Viruses come in many shapes and sizes, but these features are consistent for each viral family. As we have seen, all virions have a nucleic acid genome covered by a protective capsid. The proteins of the capsid are encoded in the viral genome, and are called capsomeres . Some viral capsids are simple helices or polyhedral “spheres,” whereas others are quite complex in structure (Figure 21.3).

In general, the capsids of viruses are classified into four groups: helical, icosahedral, enveloped, and head-and-tail. Helical capsids are long and cylindrical. Many plant viruses are helical, including TMV. Icosahedral viruses have shapes that are roughly spherical, such as those of poliovirus or herpesviruses. Enveloped viruses have membranes derived from the host cell that surrounds the capsids. Animal viruses, such as HIV, are frequently enveloped. Head-and-tail viruses infect bacteria and have a head that is similar to icosahedral viruses and a tail shaped like helical viruses.

Many viruses use some sort of glycoprotein to attach to their host cells via molecules on the cell called viral receptors . For these viruses, attachment is required for later penetration of the cell membrane only after penetration takes place can the virus complete its replication inside the cell. The receptors that viruses use are molecules that are normally found on cell surfaces and have their own physiological functions. It appears that viruses have simply evolved to make use of these molecules for their own replication. For example, HIV uses the CD4 molecule on T lymphocytes as one of its receptors (Figure 21.4). CD4 is a type of molecule called a cell adhesion molecule, which functions to keep different types of immune cells in close proximity to each other during the generation of a T lymphocyte immune response.

One of the most complex virions known, the T4 bacteriophage (which infects the Escherichia coli) bacterium, has a tail structure that the virus uses to attach to host cells and a head structure that houses its DNA.

Adenovirus, a non-enveloped animal virus that causes respiratory illnesses in humans, uses glycoprotein spikes protruding from its capsomeres to attach to host cells. Non-enveloped viruses also include those that cause polio (poliovirus), plantar warts (papillomavirus), and hepatitis A (hepatitis A virus).

Enveloped virions, such as the influenza virus, consist of nucleic acid (RNA in the case of influenza) and capsid proteins surrounded by a phospholipid bilayer envelope that contains virus-encoded proteins. Glycoproteins embedded in the viral envelope are used to attach to host cells. Other envelope proteins are the matrix proteins that stabilize the envelope and often play a role in the assembly of progeny virions. Chicken pox, HIV, and mumps are other examples of diseases caused by viruses with envelopes. Because of the fragility of the envelope, non-enveloped viruses are more resistant to changes in temperature, pH, and some disinfectants than enveloped viruses.

Overall, the shape of the virion and the presence or absence of an envelope tell us little about what disease the virus may cause or what species it might infect, but they are still useful means to begin viral classification (Figure 21.5).

Visual Connection

Which of the following statements about virus structure is true?

  1. All viruses are encased in a viral membrane.
  2. The capsomere is made up of small protein subunits called capsids.
  3. DNA is the genetic material in all viruses.
  4. Glycoproteins help the virus attach to the host cell.

Types of Nucleic Acid

Unlike nearly all living organisms that use DNA as their genetic material, viruses may use either DNA or RNA. The virus core contains the genome—the total genetic content of the virus. Viral genomes tend to be small, containing only those genes that encode proteins which the virus cannot get from the host cell. This genetic material may be single- or double-stranded. It may also be linear or circular. While most viruses contain a single nucleic acid, others have genomes divided into several segments. The RNA genome of the influenza virus is segmented, which contributes to its variability and continuous evolution, and explains why it is difficult to develop a vaccine against it.

In DNA viruses, the viral DNA directs the host cell’s replication proteins to synthesize new copies of the viral genome and to transcribe and translate that genome into viral proteins. Human diseases caused by DNA viruses include chickenpox, hepatitis B, and adenoviruses. Sexually transmitted DNA viruses include the herpes virus and the human papilloma virus (HPV), which has been associated with cervical cancer and genital warts.

RNA viruses contain only RNA as their genetic material. To replicate their genomes in the host cell, the RNA viruses must encode their own enzymes that can replicate RNA into RNA or, in the retroviruses, into DNA. These RNA polymerase enzymes are more likely to make copying errors than DNA polymerases, and therefore often make mistakes during transcription. For this reason, mutations in RNA viruses occur more frequently than in DNA viruses. This causes them to change and adapt more rapidly to their host. Human diseases caused by RNA viruses include influenza, hepatitis C, measles, and rabies. The HIV virus, which is sexually transmitted, is an RNA retrovirus.

The Challenge of Virus Classification

Because most viruses probably evolved from different ancestors, the systematic methods that scientists have used to classify prokaryotic and eukaryotic cells are not very useful. If viruses represent “remnants” of different organisms, then even genomic or protein analysis is not useful. Why?, Because viruses have no common genomic sequence that they all share. For example, the 16S rRNA sequence so useful for constructing prokaryote phylogenies is of no use for a creature with no ribosomes! Biologists have used several classification systems in the past. Viruses were initially grouped by shared morphology. Later, groups of viruses were classified by the type of nucleic acid they contained, DNA or RNA, and whether their nucleic acid was single- or double-stranded. However, these earlier classification methods grouped viruses differently, because they were based on different sets of characters of the virus. The most commonly used classification method today is called the Baltimore classification scheme, and is based on how messenger RNA (mRNA) is generated in each particular type of virus.

Past Systems of Classification

Viruses contain only a few elements by which they can be classified: the viral genome, the type of capsid, and the envelope structure for the enveloped viruses. All of these elements have been used in the past for viral classification (Table 21.1 and Figure 21.6). Viral genomes may vary in the type of genetic material (DNA or RNA) and its organization (single- or double-stranded, linear or circular, and segmented or non-segmented). In some viruses, additional proteins needed for replication are associated directly with the genome or contained within the viral capsid.

  • RNA
  • DNA
  • Rabies virus, retroviruses
  • Herpesviruses, smallpox virus
  • Single-stranded
  • Double-stranded
  • Rabies virus, retroviruses
  • Herpesviruses, smallpox virus
  • Linear
  • Circular
  • Rabies virus, retroviruses, herpesviruses, smallpox virus
  • Papillomaviruses, many bacteriophages
  • Non-segmented: genome consists of a single segment of genetic material
  • Segmented: genome is divided into multiple segments
  • Parainfluenza viruses
  • Influenza viruses

Viruses can also be classified by the design of their capsids (Table 21.2 and Figure 21.7). Capsids are classified as naked icosahedral, enveloped icosahedral, enveloped helical, naked helical, and complex. The type of genetic material (DNA or RNA) and its structure (single- or double-stranded, linear or circular, and segmented or non-segmented) are used to classify the virus core structures (Table 21.2).

Capsid Classification Examples
Naked icosahedral Hepatitis A virus, polioviruses
Enveloped icosahedral Epstein-Barr virus, herpes simplex virus, rubella virus, yellow fever virus, HIV-1
Enveloped helical Influenza viruses, mumps virus, measles virus, rabies virus
Naked helical Tobacco mosaic virus
Complex with many proteins some have combinations of icosahedral and helical capsid structures Herpesviruses, smallpox virus, hepatitis B virus, T4 bacteriophage

Baltimore Classification

The most commonly and currently used system of virus classification was first developed by Nobel Prize-winning biologist David Baltimore in the early 1970s. In addition to the differences in morphology and genetics mentioned above, the Baltimore classification scheme groups viruses according to how the mRNA is produced during the replicative cycle of the virus.

Group I viruses contain double-stranded DNA (dsDNA) as their genome. Their mRNA is produced by transcription in much the same way as with cellular DNA, using the enzymes of the host cell.

Group II viruses have single-stranded DNA (ssDNA) as their genome. They convert their single-stranded genomes into a dsDNA intermediate before transcription to mRNA can occur.

Group III viruses use dsRNA as their genome. The strands separate, and one of them is used as a template for the generation of mRNA using the RNA-dependent RNA polymerase encoded by the virus.

Group IV viruses have ssRNA as their genome with a positive polarity, which means that the genomic RNA can serve directly as mRNA. Intermediates of dsRNA, called replicative intermediates , are made in the process of copying the genomic RNA. Multiple, full-length RNA strands of negative polarity (complementary to the positive-stranded genomic RNA) are formed from these intermediates, which may then serve as templates for the production of RNA with positive polarity, including both full-length genomic RNA and shorter viral mRNAs.

Group V viruses contain ssRNA genomes with a negative polarity , meaning that their sequence is complementary to the mRNA. As with Group IV viruses, dsRNA intermediates are used to make copies of the genome and produce mRNA. In this case, the negative-stranded genome can be converted directly to mRNA. Additionally, full-length positive RNA strands are made to serve as templates for the production of the negative-stranded genome.

Group VI viruses have diploid (two copies) ssRNA genomes that must be converted, using the enzyme reverse transcriptase , to dsDNA the dsDNA is then transported to the nucleus of the host cell and inserted into the host genome. Then, mRNA can be produced by transcription of the viral DNA that was integrated into the host genome.

Group VII viruses have partial dsDNA genomes and make ssRNA intermediates that act as mRNA, but are also converted back into dsDNA genomes by reverse transcriptase, necessary for genome replication.

The characteristics of each group in the Baltimore classification are summarized in Table 21.3 with examples of each group.


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The deep evolutionary history of the new coronavirus

For the past month, news of the pandemic coronavirus, known as COVID-19, has rattled people across the U.S. and around the globe. Internationally, the nearly 1.2 million cases have resulted in more than 60,000 deaths. Businesses have shuttered, jobs have disappeared, large swaths of the population have been asked to shelter in their homes, and many others have been left homeless, hungry, and scared. Our last Evo in the news story explained how evolutionary theory helps answer important questions about the origin of the pandemic. This month we'll dig even deeper into the virus's evolutionary history and how those deep relationships relate to prospects for a vaccine.

Where's the evolution?

Structurally, viruses are little more than sacks of genetic material. They consist of DNA or RNA surrounded by a protective shell of proteins, and sometimes a layer of lipids as well. They are so small that they can't be seen with regular microscopes scientists must use techniques like electron microscopy to visualize them. Most importantly, viruses can't reproduce by themselves they invade the living cells of another organism and use the cellular machinery of that other species to copy themselves and their genetic material.

Viruses seem to occupy the gray zone between biology and chemistry. Not surprisingly, some scientists don't even consider viruses to be living things. However, being alive is not a prerequisite for experiencing evolution. Any group that varies from one individual to the next and passes on traits to descendents through reproduction (i.e., displays inheritance) can evolve. Computer programs evolve if they are designed to copy themselves with minor variations. Human languages evolve as they change slightly with culture and are passed down to children. Self-duplicating molecules in a test tube evolve as they make copying errors and introduce variation to their lineages. And so, of course, viruses &mdash whose genetic material is imperfectly copied by the machinery of their host cells &mdash also evolve.

When evolving entities like viruses pass heritable information from parent to offspring, we can depict their evolution in a tree shape, called a phylogeny. As variations are introduced and passed to offspring, new branches of the tree form. We can usually reconstruct the evolutionary history of a group by collecting information about the distribution of traits (genetic sequences, anatomical characteristics, behaviors, etc.) among lineages in that group. However, when new variations (e.g., mutations) are introduced rapid fire, it is harder to reconstruct ancient evolutionary relationships. This is because those variations are evidence, and when a lot of them occur, new changes are likely to overwrite older ones, destroying evidence of older relationships. Since viruses mutate quickly, it is very difficult to reconstruct their deep evolutionary history. Nevertheless, scientists have made a lot of progress on this challenge, especially by including information about the structure of viral proteins (and not just genetic sequences) in their analyses.

In the family tree of viruses (see below), COVID-19 fits on the branch occupied by other coronaviruses. Notice that coronaviruses are only distantly related to flu viruses, though the range of symptoms they cause is similar. Because they are not closely related, we wouldn't expect the proteins on the surface of COVID-19 to have much similarity with those of flu virus particles. Vaccines protect us from disease by teaching our immune systems to recognize and fight pathogens based on their surface proteins. In practical terms, this means that flu vaccines are designed to target different surface proteins and simply won't work against the new pandemic coronavirus, however similar the symptoms might seem. Nevertheless, keeping up to date on your flu shot is especially important during the current pandemic because people who get sick with the flu add even more burden to our stressed healthcare systems.

Evolutionary relationships among viruses and cellular life.

Click image for larger view. Credit: Science Advances

However, digging deeper into the evolutionary relationships among coronaviruses (see tree below) does reveal some cause for hope. Coronaviruses that infect humans cause a range of effects. Some, like the HKU1 strain, cause no more than a cold. Because the effects of these strains are so mild, there has been no motivation to develop vaccines against them. But others, like MERS and the SARS virus that emerged in the early 2000s, are severe diseases that kill a higher percentage of those infected than does COVID-19. SARS was stamped out a few years after it started infecting humans, but researchers did make some progress towards developing a vaccine while it was still a threat. And scientists have continued to work on a MERS vaccine, reaching hopeful milestones, though not a functional vaccine. This work on close relatives of COVID-19 may inform some efforts to develop a COVID-19 vaccine.

Evolutionary history of coronaviruses infecting humans. Note that coronaviruses infect a broad range of mammals and birds, including bats, pangolins, camels, mice, and cows. Viral lineages infecting other species are excluded from this phylogeny for clarity. Adapted from Coronoviridae Study Group of the International Committee on Taxonomy of Viruses, 2020

A critical factor in creating a vaccine to fight a new pathogen is rate of evolutionary change. Pathogens that evolve slowly (e.g., because they have a low mutation rate) remain quite similar from one infection to the next, presenting a steady target for a vaccine to aim at. However, pathogens that evolve quickly can diversify into a multitude of lineages quickly, forming a bushy evolutionary tree. This makes it difficult to design a single vaccine that can recognize and fight all the different branches of the pathogen's diverse phylogeny. HIV, for example, has the highest mutation rate of any biological lineage science has ever studied and evolves at lightning speed. For this and other reasons, we still don't have an HIV vaccine despite more than 35 years of work. Luckily, coronaviruses have a more moderate rate of evolution. While developing an effective vaccine for COVID-19 will still be a challenge, researchers are hopeful.

Understanding COVID-19 as one strain among a multitude of closely related coronaviruses can also give us an idea of how long immunity, once acquired through a vaccine or infection, might last. Coronaviruses that cause cold-like symptoms in humans trigger only short-lived immunity: you can be reinfected by the same virus in less than a year. However, for SARS and MERS &mdash strains more closely related to COVID-19 and strains that cause serious illness, as COVID-19 does &mdash immunity seems to last multiple years (though not a lifetime). While we must wait for more data to be sure, a good starting hypothesis is that immunity to COVID-19 would last several years and that we might need to be revaccinated after that.

The new coronavirus is undoubtedly frightening and dangerous &mdash but it is not unknown or unknowable. Scientific research has built a robust knowledge of viruses, with different facets of their workings illuminated by epidemiology, microbiology, genetics, and of course, evolution. Scientists around the world are bringing all this knowledge to bear as they unite in an effort to develop strategies for infection prevention, treatments, and vaccines.


Evolution of Microbes and Viruses: A New Evolutionary Paradigm?

Prokaryotes (bacteria and archaea) and viruses entered the realm of evolution with the advent of genomics. Has the comparative study of these relatively simple (compared to eukaryotes) organisms radically changed the core tenets of evolutionary biology that were first envisaged by Darwin and were augmented with the genetic foundation in the Modern Synthesis? In terms of Kuhn's concept of the development of science (Kuhn, 1962), did the study of microbial evolution engender a paradigm shift?

It is not easy to answer this question definitively, possibly because the paradigm shift model does not adequately describe the evolution of biology (regardless of whether or not it fits the evolution of physics). Probably, a more appropriate epistemological framework is that of integration, i.e., a relatively smooth incorporation of the classic concepts into the new, more general and versatile theoretical constructs. This model of the evolution of science was recognized by Kuhn himself in his later work (Kuhn, 2002) and was recently examined by O'Malley in the context of biology (O'Malley, 2012 O'Malley and Soyer, 2012). The phylogenomic study of microbes and viruses uncovered new biological realms which Darwin and even the authors of the Modern Synthesis could not possibly fathom. The modes of evolution of these relatively simple organisms that, as we now realize, have dominated the biosphere since its beginning about 4 billion years ago to this day (and into any conceivable future) are different from the evolutionary regimes of animals and plants, the traditional objects of (evolutionary) biology. The study of microbial evolution has shattered the classic idea of a single, all-encompassing tree of life by demonstrating that the evolutionary histories of individual genes are generally different. Remarkably, however, these developments have not rendered trees irrelevant as a key metaphor of evolution (O'Malley and Koonin, 2011). Rather, they have shown that the bona fide unit of tree-like evolution is an individual gene not a genome, and a “tree of life” can only be conceived as a statistical trend in the 𠇏orest” of gene trees (Koonin and Wolf, 2009b). Tree-like evolution is a fundamental implication of the binary replication of the genetic material, so it served Darwin well to use a tree as the single illustration of his book. Without, obviously, knowing anything of DNA replication, Darwin grasped the central principle of the evolution of life, descent with modification, and the tree pattern followed naturally.

Microbiology yielded the first clear-cut case of Lamarckian evolution, the CRISPR-Cas system, and subsequent re-examination of other evolutionary phenomena (in both prokaryotes and eukaryotes) has strongly suggested that the (quasi)Lamarckian modality is common and important in all evolving organisms, completing the range of evolutionary phenomena from purely stochastic (drift, Wrightean evolution) to deterministic (Lamarckian evolution). Again, these findings not so much overturned but rather expanded the vision of Darwin who seriously considered Lamarckian mechanisms as being ancillary to natural selection (only the Modern synthesis banished Lamarck).

Crucially, the study of microbial evolution presented apparently undeniable cases of evolution of evolvability such as the GTAs and the DGRs. Moreover, the discovery of bet-hedging strategies and altruistic suicide in bacteria shows that kin selection (a subject of considerable controversy in evolutionary biology) is evolvable as well. Again, as in the case of Lamarckian mechanisms, these discoveries force one to re-examine many more phenomena and realize that evolution is not limited to fixation of random variation and survival of the fittest but rather is an active process with multiple feedback loops, and that dedicated mechanisms of evolution exist and themselves evolve. This is a major generalization that substantially adds to the overall structure of evolutionary biology but one has to realize that the principle of descent with modification remains at the core of all these complex evolutionary phenomena.

We now realize that evolution of life is to a large extent shaped by the interaction (arms race but also cooperation) between genetic parasites (viruses and other selfish elements) and their cellular hosts. Viruses and related elements, with their distinctive life strategy, informational parasitism, actually dominate the biosphere both physically and genetically, and represent one of the two principal forms of life that as intrinsic to the history of the biosphere as cells are. This new dimension of evolution simply could not be perceived by Darwin or even the creators of the Modern Synthesis due to the lack of relevant data.

Thus, we are inclined to view the change in evolutionary biology brought about by phylogenomics of microbes and viruses as a case of integration rather than an abrupt departure from the paradigm of the Modern Synthesis (Figure 8). Darwin realized the importance of descent with modification and the tree pattern of evolution it implies whereas Fisher, Wright, and Haldane derived the laws of population genetics that still constitute the core of our understanding of evolution. However, recent advances, in particular those of microbial phylogenomics, added multiple, new and interconnected layers of complexity (Figure 8) such that the conceptual core is but a small part of the current big picture of evolutionary biology.

Figure 8. The conceptual structure of evolutionary biology: the Darwinian core and the new levels of complexity.