Their findings were published in Science Express last week. To view the infection process, they used genetics and cryo-electro tomography — essentially a CT scan made for objects a thousandth the diameter of a human hair — to watch as the virus inserted its genetic material into a host bacterium.
The virus, resembling a bizarre version of a golf ball on a tee, searches for the ideal location to infect its host by tottering around on fibers folded at the base of its head. Forterre proposed a hypothesis about three RNA cells which led to the current three ribosomal lineages.
According to that hypothesis, viruses contributed not only the modern dsDNA genome to the RNA cells Forterre , but also introduced the enzymes for DNA replication into the three primordial cells Forterre Viruses show a great flexibility with the chemistry of their genomes.
The modification of contemporary viral genomes is interpreted as an answer to the pressure of cellular nucleases that would otherwise digest unprotected genomes.
At the very beginning of biological evolution, this pressure might have been the incentive for viruses to play with the chemistry of nucleic acids. It is an interesting observation that DNA replication enzymes such as DNA polymerase, primase and helicase are not orthologous in Bacteria and Archaea despite the very similar DNA replication mechanisms used in both organisms. A common ancestral state is therefore unlikely. Forterre argues that they were probably derived from two different DNA viruses.
Large viruses elaborate complex virus-induced structures in the infected host cell, including an intracellular viral factory which somewhat resembles a cell nucleus Suzan-Monti et al. This has led to the speculation that the eukaryotic nucleus might be a viral invention Claverie In mimivirus-infected cells, researchers found virus production sites viral factories which release mature progeny viral particles into the cell.
Recently, a much smaller virus was seen associated with the mimivirus intracellular viral factory. It was called Sputnik and had an 18 kb genome La Scola et al. Most of its genes had no database matches while three were related to mimivirus proteins.
Sputnik cannot grow on uninfected amoeba. However, when it grows in mimivirus-infected amoeba, it substantially decreases the yield of mimivirus and the lysis of the amoeba. Notably, this is the first virus which grows on another virus. Their small genomes do not encode for a capsid protein and the satellite virus relies on a helper virus for encapsidation.
Virologists have also shown that defective interfering particles from negative strand RNA animal viruses reduce the infectivity of the helper virus Roux However, in that case a truncated genome of the helper virus lacking the viral RNA polymerase gene competed very efficiently with the replication of the full-sized genome. All these discoveries demonstrate that we have to account for virus—virus competition when describing the virus—cell interaction.
The jelly-roll capsid protein is an interesting viral hallmark gene. The two jelly rolls have the same topology, but no apparent sequence conservation. If they are the result of gene duplication, the event must be very ancient. This protein associates in trimers and forms a basic structural element composing the viral capsid. When analysing this protein in the E. The similarity between phage and adenovirus goes even farther.
Both capsids show the same lattice type. Pentameric proteins occupy the vertices of their capsids, to which fibre proteins are attached. Both viral genomes are linear dsDNA with inverted terminal repeats. The researchers judged that these observations cannot be explained by convergence and they argued for a very ancient link between viruses infecting two distinct domains of life.
They predicted that jelly roll proteins will be found in viruses infecting other forms of cellular life. Soon it was shown that a Phycodnavirus that infects Chlorella a unicellular photosynthetic alga had a capsid protein similar to that of phage PRD1 Nandhagopal et al.
Similarities went beyond this shared protein fold. The algal virus, when attached to its hosts, digests the cell wall around the attachment point, injects its DNA and leaves its empty capsid on the cell surface. This infection mechanism is quite unusual for a virus infecting eukaryotes, but typical for viruses infecting prokaryotes.
This initial prediction has been confirmed as the same capsid fold has been described in an archaeal virus that infects Sulfolobus , which lives in an extreme environment characterized by low pH and high temperatures Khayat et al.
These observations are now a strong argument for a common origin of the capsid in viruses infecting all three domains of cellular life. Like the shared gene map argument, structural biology provides new tools in the exploration of distant evolutionary relationships, which are so ancient that all sequence similarity has been erased. Other traits of the virus such as recognition and multiplication in a given host necessitate adaptation of the virus to the cellular host. Proteins involved in that task tend to be acquired horizontally, typically from the host or from other viruses exploiting the same host.
This hypothesis fits nicely with the genome categorization of viral genes and ideas from Forterre on viral evolution. Structural biologists have also identified a second lineage of viral capsid proteins that is likewise distributed across all three domains of life. A closely related fold is found in the head proteins from E. A related protein fold was identified in a virus-like particle from the Archaeon Pyrococcus furiosus and in animal herpesvirus Akita et al. The wide phyletic distribution of a second viral protein fold suggests that the ancestor of the three domains Commonote might already have been infected by at least two ur-viruses defining two distinct lineages.
The morphological structure of bacterial viruses is quite peculiar. The prototype is represented by a capsid containing the viral genome, a tail for injecting the genome into the bacterial cell and a base plate with tail fibres for the identification of the appropriate target cell Miller et al.
This structure combines the advantage of a genuine gene container, with a mechanical conduit for guiding the DNA into the target cell, linked to a sophisticated sensor, which differentiates target from non-target cells.
The tailed virus model is so efficient that nearly every physical viral particle is also an infectious virus. In morphologically less well-defined animal viruses, frequently only one out of physical particles is actually an infectious virus. It is not obvious from what cellular material these sophisticated base plate structures could have been derived Kanamaru et al. Some phages show a distinctly different morphology including tail-less capsids, membrane-enveloped phage particles and filamentous phages.
However, the selective advantage of the tailed phage construction model is overwhelming as more than 96 per cent of all described bacterial viruses are tailed phages Caudovirales Ackermann Viruses from the other two domains of life are morphologically less uniform.
Caudovirales are also found in the Euryarchaeota subgroup of Archaea Pfister et al. Some Euryarchaeota also have a high percentage of genes of probable bacterial origin, leading to the suggestion that Caudovirales entered Euryarchaeota by interdomain genetic exchanges.
In the other branch of Archaea, the Crenarchaeota, a bewildering morphological diversity of viruses, was identified Prangishvili et al. Strange archaeal viruses resembled spindles Fuselloviridae or are lemon-shaped. In Crenarchaeota, there are furthermore bottle-shaped Ampullaviridae and droplet-shaped Guttaviridae viruses, others are linear viruses without Rudiviridae and with lipid-containing envelopes Lipothrixviridae.
Some linear viruses end with a claw, which clamps the virus onto the pili of the archaeal host. There are also enveloped spherical viruses Globuloviridae and spherical archaea viruses that contain internal membranes like Tectivirus PRD1, infecting E.
It is not clear how this morphological diversity of viruses could have originated in the cellular world. Viruses from Crenarchaeota display unique morphologies and their genomes contain mainly unknown genes.
For example, Acidianus bottle-shaped virus, an Ampullavirus, showed over its 57 ORFs only three which had significant database hits Peng et al. Also in some bacterial viruses e. Mycobacteria phages , the majority of the ORFs are novel Pedulla et al.
One might argue that much more of the global bacterial metagenome has been sampled, while the viral metagenome is still mostly unexplored. However, substantial metagenome analyses of viral DNA sequences have recently been conducted in various environments.
One large study comprised 15 million sequences from nine biomes, terrestrial and aquatic Dinsdale et al. The most extensively explored system was ocean water collected over a decade and representing the major oceanic regions of the world.
In the largest of the ocean studies, more than 91 per cent of the sequences from the viral DNA fraction did not have a significant hit in the sequence databases Angly et al. From this observation, we have to conclude that the viral DNA sequence sphere is very large. The first big surprise was the discovery of large numbers of viruses in coastal water. In eutrophic estuarine water, 10 7 viral particles were counted per millilitre of water. This is 10 times the amount of bacteria in this ecosystem.
Viruses are not only numerous, they are also a major cause of microbial mortality in the sea, rivaled only by grazing from protists Breitbart et al. In addition, viruses power the microbial loop that maintains nutrients in the microbial world, preventing their flow into the marine food chain. Therefore, viruses play a major role in biogeochemistry. This role is not limited to the open sea. The deep-sea floor covers approximately 65 per cent of the Earth's surface and the prokaryotic biomass in the top 10 cm of the ocean sediment contains an estimated half of the total microbial carbon on Earth.
Recent ecological surveys documented a deep viral impact on this benthic ecosystem Danovaro et al. If one combines the large number of ORFans in viral metagenome analyses and the sheer number of viruses in the biosphere, it is possible that the viral sequence space exceeds that of their prokaryotic hosts in size. These data are simply not compatible with the older concept that the viral genes escaped from cells.
Classically, phages and bacteria were interpreted in the predator—prey framework. Phages could not extinguish the host cells because they relied on the translation and energy production capacities of their bacterial hosts. Should they wipe out their bacterial host, the phage would also go extinct. In contrast, it is not clear why bacteria should not force phages into extinction. The conundrum is normally answered by reference to an arms race between phages and bacteria, which can be inferred from the analysis of the highly variable genes.
Genes encoding restriction enzymes as defence against foreign DNA intrusion and lipopolysaccharides as phage receptor are hotspots of E.
However, this cannot be the whole story. During in vitro co-evolution experiments, phages frequently lose the race against bacteria. Are there reasons that bacteria live under natural conditions better with phages than without them? Indeed, in recent years, phage—bacterium interaction has received a much more positive interpretation than previously.
Phages were identified as a source of bacterial genetic diversity. When different bacterial strains, belonging, for example, to the same species of lactic acid bacteria, are compared, they typically differ for approximately 10 per cent of their gene content Berger et al. The host specificity of phages can be an advantage over broad-spectrum antibiotics, which can wipe out both pathogenic and beneficial bacteria, Ebner says.
The paper is published in the Journal of Animal Science. Source: Purdue University. Search for:. Science Health Culture Environment. Share this Article. You are free to share this article under the Attribution 4.
If the virions are released by bursting the cell, the virus replicates by means of a lytic cycle [link]. An example of a lytic bacteriophage is T4, which infects Escherichia coli found in the human intestinal tract. Sometimes, however, a virus can remain within the cell without being released. For example, when a temperate bacteriophage infects a bacterial cell, it replicates by means of a lysogenic cycle [link] , and the viral genome is incorporated into the genome of the host cell.
When the phage DNA is incorporated into the host cell genome, it is called a prophage. Viruses that infect plant or animal cells may also undergo infections where they are not producing virions for long periods. An example is the animal herpesviruses, including herpes simplex viruses, the cause of oral and genital herpes in humans.
In a process called latency , these viruses can exist in nervous tissue for long periods of time without producing new virions, only to leave latency periodically and cause lesions in the skin where the virus replicates.
Even though there are similarities between lysogeny and latency, the term lysogenic cycle is usually reserved to describe bacteriophages.
Latency will be described in more detail below. As a protein in the viral capsid binds to its receptor on the host cell, the virus may be taken inside the cell via a vesicle during the normal cell process of receptor-mediated endocytosis.
An alternative method of cell penetration used by non-enveloped viruses is for capsid proteins to undergo shape changes after binding to the receptor, creating channels in the host cell membrane. Enveloped viruses also have two ways of entering cells after binding to their receptors: receptor-mediated endocytosis, or fusion. Many enveloped viruses enter the cell by receptor-mediated endocytosis in a fashion similar to some non-enveloped viruses. On the other hand, fusion only occurs with enveloped virions.
These viruses, which include HIV among others, use special fusion proteins in their envelopes to cause the envelope to fuse with the plasma membrane of the cell, thus releasing the genome and capsid of the virus into the cell cytoplasm. After making their proteins and copying their genomes, animal viruses complete the assembly of new virions and exit the cell.
On the other hand, non-enveloped viral progeny, such as rhinoviruses, accumulate in infected cells until there is a signal for lysis or apoptosis, and all virions are released together. As you will learn in the next module, animal viruses are associated with a variety of human diseases.
Some of them follow the classic pattern of acute disease , where symptoms get increasingly worse for a short period followed by the elimination of the virus from the body by the immune system and eventual recovery from the infection.
Examples of acute viral diseases are the common cold and influenza. Other viruses cause long-term chronic infections , such as the virus causing hepatitis C, whereas others, like herpes simplex virus, only cause intermittent symptoms. Still other viruses, such as human herpesviruses 6 and 7, which in some cases can cause the minor childhood disease roseola, often successfully cause productive infections without causing any symptoms at all in the host, and thus we say these patients have an asymptomatic infection.
In hepatitis C infections, the virus grows and reproduces in liver cells, causing low levels of liver damage. The damage is so low that infected individuals are often unaware that they are infected, and many infections are detected only by routine blood work on patients with risk factors such as intravenous drug use.
On the other hand, since many of the symptoms of viral diseases are caused by immune responses, a lack of symptoms is an indication of a weak immune response to the virus. This allows for the virus to escape elimination by the immune system and persist in individuals for years, all the while producing low levels of progeny virions in what is known as a chronic viral disease. Chronic infection of the liver by this virus leads to a much greater chance of developing liver cancer, sometimes as much as 30 years after the initial infection.
As already discussed, herpes simplex virus can remain in a state of latency in nervous tissue for months, even years. Under certain conditions, including various types of physical and psychological stress, the latent herpes simplex virus may be reactivated and undergo a lytic replication cycle in the skin, causing the lesions associated with the disease.
Once virions are produced in the skin and viral proteins are synthesized, the immune response is again stimulated and resolves the skin lesions in a few days by destroying viruses in the skin. As a result of this type of replicative cycle, appearances of cold sores and genital herpes outbreaks only occur intermittently, even though the viruses remain in the nervous tissue for life.
Latent infections are common with other herpesviruses as well, including the varicella-zoster virus that causes chickenpox. Some animal-infecting viruses, including the hepatitis C virus discussed above, are known as oncogenic viruses : They have the ability to cause cancer.
These viruses interfere with the normal regulation of the host cell cycle either by either introducing genes that stimulate unregulated cell growth oncogenes or by interfering with the expression of genes that inhibit cell growth.
Cancers known to be associated with viral infections include cervical cancer caused by human papillomavirus HPV [link] , liver cancer caused by hepatitis B virus, T-cell leukemia, and several types of lymphoma.
Link to Learning. Visit the interactive animations showing the various stages of the replicative cycles of animal viruses and click on the flash animation links. You have already learned about one of these, the tobacco mosaic virus. As plant cells have a cell wall to protect their cells, these viruses do not use receptor-mediated endocytosis to enter host cells as is seen with animal viruses.
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