The virus travels through neurons in the peripheral nervous system to the central nervous system, where it impairs brain function, and then travels to other tissues. The virus can infect any mammal, and most die within weeks of infection. Smallpox is a human virus transmitted by inhalation of the variola virus, localized in the skin, mouth, and throat, which causes a characteristic rash. Before its eradication in , infection resulted in a 30 to 35 percent mortality rate.
Virus Classification by Capsid Structure 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 Transmission electron micrographs of various viruses show their capsid structures.
The capsid of the a polio virus is naked icosahedral; b the Epstein-Barr virus capsid is enveloped icosahedral; c the mumps virus capsid is an enveloped helix; d the tobacco mosaic virus capsid is naked helical; and e the herpesvirus capsid is complex. Forgot password? Show password. Create an account Register. Rabies virus, retroviruses Herpesviruses, smallpox virus. Interestingly, conservation of folds in viral proteins has begun to highlight possible common ancestries that could never be inferred from genome sequence data.
A striking example is domain duplication of the beta jelly roll motif which gives rise to the pseudo-sixfold symmetry of trimeric hexon capsomeres in adenovirus. This is also found in viruses that infect insects, Gram-positive and Gram-negative bacteria and extremophile archaea. Viruses assemble their capsids from surprisingly few distinct protein folds, such that convergent evolution seems highly implausible.
A recent study has investigated viral origins by analysis of the evolution and conservation of protein folds in the structural classification of proteins SCOP database. This work identified a subset of proteins that are unique to viruses. The authors conclude that viruses most likely originated from early RNA-containing cells. If viruses made an evolutionary leap away from the cellular form, casting off its weighty metabolic shackles to opt for a more streamlined existence, did they cease to be life?
Have they reverted to mere chemistry? They all have surprisingly complex replication life cycles, however; they are exquisitely adapted to deliver their genomes to the site of replication and have precisely regulated cascades of gene expression.
Viruses also engineer their environment, constructing organelles within which they may safely replicate, a feature they share with other intracellular parasites. Fundamental to the argument that viruses are not alive is the suggestion that metabolism and self-sustaining replication are key definitions of life. Viruses are not able to replicate without the metabolic machinery of the cell.
No organism is entirely self-supporting, however — life is absolutely interdependent. There are many examples of obligate intracellular organisms, prokaryote and eukaryote that are critically dependent on the metabolic activities of their host cells.
Humans likewise depend on the metabolic activity of nitrogen-fixing bacteria and photosynthetic plants along with that of our microbiota. There are very few if any forms of life on Earth that could survive in a world in which all chemical requirements were present but no other life. So, what does define life? Some have argued that the possession of ribosomes is a key ingredient. This draws a neat distinction between viruses and obligate intracellular parasites such as Chlamydia and Rickettsia.
This definition also confers the status of life on mitochondria and plastids, however. Viruses can be classified into archaeoviruses, bacterioviruses, and eukaryoviruses according to the taxonomy of the infected host. The host-constrained perception of viruses implies preference of genetic exchange between viruses and cellular organisms of their host superkingdoms and viral origins from host cells either via escape or reduction.
However, viruses frequently establish non-lytic interactions with organisms and endogenize into the genomes of bacterial endosymbionts that reside in eukaryotic cells. Such interactions create opportunities for genetic exchange between viruses and organisms of non-host superkingdoms. Here, we take an atypical approach to revisit virus-cell interactions by first identifying protein fold structures in the proteomes of archaeoviruses, bacterioviruses, and eukaryoviruses and second by tracing their spread in the proteomes of superkingdoms Archaea, Bacteria, and Eukarya.
The exercise quantified protein structural homologies between viruses and organisms of their host and non-host superkingdoms and revealed likely candidates for virus-to-cell and cell-to-virus gene transfers. Unexpected lifestyle-driven genetic affiliations between bacterioviruses and Eukarya and eukaryoviruses and Bacteria were also predicted in addition to a large cohort of protein folds that were universally shared by viral and cellular proteomes and virus-specific protein folds not detected in cellular proteomes.
These protein folds provide unique insights into viral origins and evolution that are generally difficult to recover with traditional sequence alignment-dependent evolutionary analyses owing to the fast mutation rates of viral gene sequences. Depending on the nature of the infected host, viruses can be broadly classified into three major groups, archaeoviruses, bacterioviruses Krupovic et al. While host jumps are common Longdon et al.
This has been confirmed by recent studies revealing strong biases in the distribution of viral replicon types in superkingdoms such as the paucity of discovered RNA and retrotranscribing viruses in prokaryotes and their abundance and diversity in eukaryotic species such as mammals and vertebrates Nasir et al.
The highly specific nature of virus-host interactions logically constrains genetic exchange to occur more frequently between the interacting partners. For example, bacterioviruses are known to capture bacterial genes involved in toxins and photosynthesis Canchaya et al.
Similarly, eukaryoviruses often capture genes involved in antiviral immunity from eukaryotic cells Elde and Malik, ; Rappoport and Linial, Virus-host affiliations however are largely established by observing the cytopathic effects of viral infection or by microscopy detection of virion particles.
These properties relate to the lytic mode of viral reproduction that has historically remained on focus due to the noxious effects that lysis has on human health, livestock, and agriculture. However, viruses can also frequently endogenize by integration into cellular genomes Feschotte and Gilbert, , sometimes providing useful novel genes to make them evolutionarily competitive Cornelis et al.
Moreover, many viruses either infect bacterial symbionts of eukaryotic cells e. These virus-cell interactions are largely non-lytic in nature and because they do not yield the classic phenotypic effects of viral infection, have likely remained underestimated through established methods of virus discovery reviewed in Nasir et al.
The study therefore offered unique insights into virus-cell interactions that extend beyond their known hosts and identified viruses of endosymbiotic bacteria as interesting examples of vectors with genetic material from non-host superkingdoms. The comparative exercise of tracing the spread of each viral FSF in cellular proteomes was made explicit with an f -value representing the fraction of cellular proteomes encoding individual FSFs see Methods.
The f -values of viral FSFs in cellular proteomes and their reported biochemical functions were then used to postulate hypotheses regarding the direction of gene transfer, virus-to-cell or cell-to-virus see Figure 1 for demonstration. For example, an FSF with a viral hallmark function e. This approach of inferring the likely direction of gene transfer is thus similar to considering anomalous phylogenetic distributions of genes in closely related species as more likely a result of HGT rather than vertical inheritance and loss.
The tracings yielded unique insights into genetic transfers between viruses and cells, highlighted the quantitatively greater cross-superkingdom genetic exchange occurring between bacterioviruses and eukaryotes and eukaryoviruses and bacteria, and supported models of viral origins from ancient cells Nasir et al.
The genetic crosstalk between viral and cellular proteomes that we uncover with this comparative genomics approach presents a more global picture for evolutionary understanding of virus-cell interactions that goes beyond the perceived textbook definitions of virus hosts Nasir et al.
Figure 1. Demonstration of virus-to-cell and cell-to-virus HGT events. Ten genomes are displayed as colored closed disks each for Archaea black , Bacteria blue , Eukarya green , and viruses. Seven out of 10 viral genomes encode different virus hallmark FSFs with incidence represented by different shades of red such as those involved in virion synthesis and capsid assembly.
In turn, any of the cellular FSFs that are widespread in cells i. A total of 98, , and FSFs were detected in the proteomes of 62 archaeoviruses , 1, bacterioviruses , and 2, eukaryoviruses Table S1 , respectively Figure 2. Figure 2. Sharing of protein structural domains between viral and cellular proteomes. The Venn diagrams illustrate the number of FSFs detected in the proteomes of archaeoviruses, bacterioviruses , and eukaryoviruses and their distributions in the proteomes of superkingdoms Archaea A , Bacteria B , and Eukarya E.
V represents virus-specific FSFs Table 2. Under the expected host-constrained evolution model of viral lineages, viruses of any superkingdom are expected to share more FSFs with organisms of their host superkingdom rather than with organisms of other superkingdoms.
Remarkably, the 29 FSFs shared exclusively between bacterioviral and bacterial proteomes included several viral hallmark proteins involved in phage virus assembly such as the gp9 and gp10 proteins, head-binding, head-to-tail joining, head decoration, and tail proteins, along with the major coat proteins of ssDNA harboring bacterioviruses Inoviridae and the dimerization domain of bacteriophage T4 recombination endonuclease VII Table 1.
In addition, the coiled-coiled domain of bacterial neurotoxin involved in host virulence was also detected. Interestingly, the majority of FSFs in group B had f -values close to 0 indicating their rare presence in bacterial proteomes Table 1.
Collectively, therefore, the enrichment of the B Venn group in viral hallmark functions with negligible presence in bacterial proteomes suggests that these genes were likely acquired by bacterial cells from viruses via virus-to-cell HGT, a phenomenon that has been assumed to be relatively less frequent than cell-to-virus HGT Moreira and Lopez-Garcia, , though now increasingly being revisited Forterre, Similarly, viral hallmark proteins such as the viral capsid and coat-related proteins e.
These viral hallmark proteins shared exclusively between eukaryoviruses and eukaryotes could therefore also represent episodes of virus-to-cell gene transfer.
In summary, a large number of FSFs shared exclusively between viruses and their host genomes had rare presence in hosts and were involved in virus-hallmark functions suggesting these genes likely originated in viral lineages and were later transferred to their host cells.
While the data of Figure 2 indicated significant levels of genetic exchange restricted between viruses and their known host superkingdoms, some bacterioviral and eukaryoviral FSFs were also shared with Eukarya and Bacteria, respectively archaeoviruses shared no domains exclusively with either Bacteria or Eukarya Figure 2 , Tables S2 — S4.
It is however indeed intriguing to note that these FSFs were present in eukaryotic proteomes, especially because the capsid is considered to be a virus hallmark Benson et al. Its presence in eukaryoviruses but not in eukaryotic proteomes! In turn, the 5 FSFs shared exclusively between eukaryoviruses and bacterial proteomes the B Venn group included capsid proteins Outer capsid protein sigma 3 and other virus and cell-like proteins likely indicating a mixed ancestry Table S4.
Finally, the BE Venn group for archaeoviruses , the AE group for bacterioviruses , and the AB group for eukaryoviruses may also represent genetic exchanges occurring between viruses and non-host superkingdoms.
For archaeoviruses , the d. In turn, only one bacterioviral FSF d. Figure 3. The structural domain composition of the BE Venn group in bacterioviruses and eukaryoviruses. B Boxplots display the distribution of f -values number of proteomes in a superkingdom encoding an FSF divided by the total number of proteomes in that superkingdom for BE FSFs unique to bacterioviruses , unique to eukaryoviruses , and common to both the bacterial and eukaryal proteomes see also Table S5.
P -values were calculated from two-sample Welch t -tests. We hypothesize that bacterioviruses and eukaryoviruses acquired BE FSFs directly from their host cells i. For example, FSF d. Therefore, closer inspection of BE FSFs in bacterioviruses indicated that both sources of origin could be considered likely, especially when accounting for the relative preference of bacterial species to become endosymbionts of eukaryotes and considering mechanical similarities between bacterial and eukaryotic cells read below.
To test, we divided eukaryoviruses into five subgroups representing viruses of fungi, plants, metazoa, protozoa, and invertebrates-plants viruses that can replicate in both plants and insect vectors , as defined by the NCBI Viral Genomes Resource Figure 4. FSF distributions of the five subgroups of eukaryoviruses were mapped to the seven Venn groups already defined for eukaryoviruses Figure 2.
Interestingly, only 27 viruses were associated to protozoa. These viruses encoded a total of FSFs the second largest amongst the five eukaryoviral subgroups after FSFs of metazoan viruses. Similarly, free-living amoeba e. These two eukaryotic host subgroups therefore provide ample opportunities for eukaryoviruses to exchange genetic material either directly with bacterial proteomes or through prophages integrated in bacterial genomes.
Figure 4. Breakdown of the FSFs detected in eukaryoviruses. Eukaryoviruses were divided into viruses of plants included all plants, blue-green algae, and diatoms , metazoa vertebrates and invertebrates , protozoa animal-like protists , fungi, and a group that includes invertebrates and plants IP.
For each subgroup, bars indicate the percentage of FSFs present in one of the seven Venn groups listed on the right see also Figure 2 and the percentage of virus-specific FSFs. Numbers on bars indicate actual count. The ABE group was the largest Venn group for viruses of the three superkingdoms i. It suggests two possible scenarios. For example, ABE FSFs can be transferred directly from Archaea to archaeoviruses , from Bacteria to bacterioviruses , and Eukarya to eukaryoviruses , in addition to indirect cross-superkingdom genetic transfers.
Figure 5. This classification enabled evaluation of virus-to-virus HGTs in contrast to either virus-to-cell or cell-to-virus candidate HGT events postulated above. The next larger groups included e and b Figure 6. These could represent direct HGT events from bacterial proteomes to bacterioviruses and eukaryal proteomes to eukaryoviruses , respectively. Figure 6. Breakdown of pooled non-redundant viral ABE FSFs see text into seven possible Venn groups for archaeoviruses, bacterioviruses , and eukaryoviruses.
Numbers on bars indicate actual count see also Table S6. A total of 66 ABE FSFs were detected in the proteomes of archaeoviruses, bacterioviruses , and eukaryoviruses Venn group abe , again enriched in cell-like functions highlighted in Table S6.
While significant cross-superkingdom indirect genetic exchange cannot be ruled out, the possibility of the same HGT event occurring three times independently and in different ecological habitats should be considered unlikely. The origin of abe FSFs is therefore better and more parsimoniously reconciled with an origin of modern viral lineages in ancient cells that existed prior to the diversification of cellular life and experienced high levels of genome reduction Nasir et al. One interesting observation was the existence of only 2 FSFs belonging to the ae group.
Under this scenario, one should expect stronger affiliation of eukaryoviruses with archaeoviruses , which however does not materialize in the FSF data. 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 , 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 , 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. Most virions , or single virus particles, are very small, about 20 to nanometers in diameter.
However, some recently discovered viruses from amoebae range up to 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 s that scientists got their first good view of the structure of the tobacco mosaic virus TMV Viruses: Introduction: Figure 1 , discussed in the previous chapter, and other viruses Figure 1, below.
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. 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.
There are current evolutionary scenarios that may explain the origin of viruses. 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 that escaped from a host cell.
A third hypothesis, the self-replicating hypothesis, suggests that viruses may have originated from self-replicating entities similar to transposons or other mobile genetic elements. 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. 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.
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.
In general, the capsids of viruses are classified into four groups: helical, icosahedral, enveloped, and head-and-tail. Helical capsids are long and cylindrical.
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