Host cell virus

This way, the virus can exit the host cell without killing it. What advantage does the virus gain by keeping the host cell alive? Watch this video on viruses, identifying structures, modes of transmission, replication, and more.

This feature of a virus makes it specific to one or a few species of life on Earth. On the other hand, so many different types of viruses exist on Earth that nearly every living organism has its own set of viruses trying to infect its cells.

Even prokaryotes, the smallest and simplest of cells, may be attacked by specific types of viruses. In the following section, we will look at some of the features of viral infection of prokaryotic cells. As we have learned, viruses that infect bacteria are called bacteriophages Figure 2. Archaea have their own similar viruses. Phage particles must bind to specific surface receptors and actively insert the genome into the host cell. The complex tail structures seen in many bacteriophages are actively involved in getting the viral genome across the prokaryotic cell wall.

When infection of a cell by a bacteriophage results in the production of new virions, the infection is said to be productive. If the virions are released by bursting the cell, the virus replicates by means of a lytic cycle Figure 3.

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 Figure 3 , 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 sometimes 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 in the next section. However, there are also plant viruses in most other virus categories. Unlike bacteriophages, plant viruses do not have active mechanisms for delivering the viral genome across the protective cell wall.

For a plant virus to enter a new host plant, some type of mechanical damage must occur. This damage is often caused by weather, insects, animals, fire, or human activities like farming or landscaping.

Movement from cell to cell within a plant can be facilitated by viral modification of plasmodesmata cytoplasmic threads that pass from one plant cell to the next.

Additionally, plant offspring may inherit viral diseases from parent plants. The transfer of a virus from one plant to another is known as horizontal transmission , whereas the inheritance of a virus from a parent is called vertical transmission. Symptoms of viral diseases vary according to the virus and its host Table 1.

One common symptom is hyperplasia , the abnormal proliferation of cells that causes the appearance of plant tumors known as galls. Other viruses induce hypoplasia , or decreased cell growth, in the leaves of plants, causing thin, yellow areas to appear. Still other viruses affect the plant by directly killing plant cells, a process known as cell necrosis. Other symptoms of plant viruses include malformed leaves; black streaks on the stems of the plants; altered growth of stems, leaves, or fruits; and ring spots, which are circular or linear areas of discoloration found in a leaf.

Plant viruses can seriously disrupt crop growth and development, significantly affecting our food supply. They are responsible for poor crop quality and quantity globally, and can bring about huge economic losses annually.

Others viruses may damage plants used in landscaping. Some viruses that infect agricultural food plants include the name of the plant they infect, such as tomato spotted wilt virus, bean common mosaic virus, and cucumber mosaic virus. In plants used for landscaping, two of the most common viruses are peony ring spot and rose mosaic virus. There are far too many plant viruses to discuss each in detail, but symptoms of bean common mosaic virus result in lowered bean production and stunted, unproductive plants.

In the ornamental rose, the rose mosaic disease causes wavy yellow lines and colored splotches on the leaves of the plant. Animal viruses, unlike the viruses of plants and bacteria, do not have to penetrate a cell wall to gain access to the host cell. The virus may even induce the host cell to cooperate in the infection process. 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.

This process is mainly driven by the attractive electrostatics interaction between the positive charges on capsid proteins and the negative charges on the genome. Despite its importance and many decades of intense research, how the virus selects and packages its native RNA inside the crowded environment of a host cell cytoplasm in the presence of an abundance of nonviral RNA and other anionic polymers has remained a mystery.

In this paper, we perform a series of simulations to monitor the growth of viral shells and find the mechanism by which cargo—coat protein interactions can impact the structure and stability of the viral shells.

We show that coat protein subunits can assemble around a globular nucleic acid core by forming nonicosahedral cages, which have been recently observed in assembly experiments involving small pieces of RNA. We find that the resulting cages are strained and can easily be split into fragments along stress lines.

This suggests that such metastable nonicosahedral intermediates could be easily reassembled into the stable native icosahedral shells if the larger wild-type genome becomes available, despite the presence of a myriad of nonviral RNAs.

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More by Sanaz Panahandeh. More by Siyu Li. More by Bogdan Dragnea. Specifically, viruses depend on host cells for: 1 energy, mainly in the form of nucleoside triphosphates, for polymerization involved in genome and viral protein synthesis; 2 a protein-synthesizing system for synthesis of viral proteins from viral mRNAs some viruses also require host enzymes for posttranslational modification of their proteins; e.

Even though the dependence on host cell functions varies between virus groups and largely relates to genome complexity, nowhere in the biosphere is genome replication accomplished with greater economy and simplicity than among viruses. Accordingly, viral genomes contain regulatory RNA elements that promote, regulate, and coordinate these molecular processes. The central role played by viral genomes is frequently executed by viral or host cell proteins that interact with these genomes, but other partners include other RNA molecules e.

Together, protein and RNA factors interact with cellular pathways to allow viruses to successfully hijack and customize the host cell machinery for virus production. As a result, viruses and their hosts have been involved in a long-standing battle of adaptation and counter-adaptation for gene expression and nucleic acid synthesis. In this chapter, we address genome replication strategies including the diverse strategies that exploit the biology of the hosts, control gene expression, and ensure preferential propagation of the virus.

Work with bacteriophages identified the essential phases of virus replication. The process, beginning with entry of the virus into the host cell to the release of progeny viruses, is referred to as the replication cycle. The replication cycle of all viruses involves three key phases: initiation of infection, genome replication and expression, and finally, egress or release of mature virions from the infected cell.

From the perspective of the virus, the purpose of viral replication is to allow production and survival of its kind. By generating abundant copies of its genome and packaging these copies into virions, the virus is able to continue infecting new hosts.

All viruses must therefore express their genes as functional mRNAs early in infection in order to direct the cellular translational machinery to synthesize viral proteins. The pathways leading from genome to message vary among different viruses Fig. Viral genomes provide examples of almost every structural variation imaginable.

These categories are further divided on the basis of distinct modes of transcription. Summary of replication and transcription modes of different classes of viruses. Both pathways require enzymatic activities that are not usually found in uninfected host cells and as a result, these viruses code for the requisite enzymes, which are either expressed early in infection or they are copackaged with the viral genome during the assembly of virions in preparation for the next round of infection.

The virus genome integrates into the host genome and can be passed from parent to offspring should integration occur in germline cells. The integrated virus genome, referred to as a provirus, is transcribed as a cellular gene some may require splicing and translated by the cellular synthesis machinery on export to the cytoplasm. It should be noted that in all these examples, the balance between the processes of transcription and genome replication must be properly maintained to allow efficient viral proliferation.

It appears that the transition occurs by the 1 action of trans -acting proteins that are either absent, or at low levels in virions, but which accumulate over the course of infection; 2 regulatory role of promoter RNA secondary structure along with the action of specific viral e.

Many use host enzymes for these processes, while some larger viruses code for their own enzymes. Cellular splicing machinery typically generates mature viral mRNAs. The switch from transcription to replication, that is the switch from antigenome production to genomic nucleic acid for packaging, is highly regulated, and unlike RNA viruses, there is the strict demarcation with respect to timing of genomic DNA replication. Early genes, which code for catalytic e.

Late genes that code for the structural components of the capsid and envelope are transcribed only after viral DNA replication. Large DNA viruses, for example, members of Herpesviridae, Adenoviridae , and Poxviridae , and giant viruses, are among those viruses that encode most of their own proteins for replication. Proteins encoded by these viruses are those involved in recognition of the origin of replication, DNA-binding proteins, helicases and primases, DNA polymerase and accessory proteins, exonucleases, thymidine kinase, and dUTPase.

Small DNA viruses, for example, Papillomaviridae, Polyomaviridae , and Parvoviridae , do not encode the entire repertoire of proteins required for viral replication because of their limited genome size. They do, however, encode proteins that usurp and control cellular activities. Viruses that do not replicate in the nucleus and do not have access to host polymerases, typically encode their own polymerases for replication. RT is virus-encoded as the host cell does not require this enzyme for its nuclear metabolism.

Although high fidelity of virus genome replication is crucial for the long-term survival of viruses, some polymerases are less faithful than others when incorporating the correct nucleotide during replication. The rate by which mutations occur is universally determined as the number of nucleotide substitutions per base per generation.

DNA viruses experience low mutation rates. This is because of the proofreading ability of the polymerase. With the exception of nidoviruses, the replicative enzymes of RNA viruses RdRps lack proofreading ability and these viruses exhibit the highest mutation rates.

Not all mutations generated will persist in a virus population, however. Mutations may be neutral or silent because of genetic code redundancy and those that interfere with viral replicative mechanisms are eliminated from the viral population.

Mutations that do not affect essential viral functions may persist and eventually become fixed within the viral population see Chapter 4: Origins and Evolution of Viruses. Unlike cellular DNA and RNA polymerases, which require oligonucleotides to initiate nucleic acid synthesis, viral polymerases initiate genome replication using a variety of mechanisms, that presumably reflect their adaptation to the host cell.

Nucleic acid synthesis by polymerases is divided into three phases: initiation, elongation, and termination. Both virus genome transcription and mRNA synthesis occur in three stages. Two different start sites are used in the synthesis of mRNA and viral genome RNA in a primer-independent de novo , or a primer-dependent mechanism. Structures in the polymerase or conformational changes apparently contribute to the process. Another capping mechanism used by negative-sense RNA viruses e.

Poliovirus RdRp, for example, adds about nucleotides and so in a single-binding event it can synthesize the entire genome. Termination leads to the release of the newly synthesized RNA strand and the dissociation of the polymerase from the template. Transcription termination involves secondary structure mechanisms or in eukaryotic cells, RNA signals direct polyadenylation and termination. Unlike polyadenylation of host mRNAs, which is carried out by a specific poly A polymerase, polyadenylation of viral mRNAs is catalyzed by the viral polymerase.

In nonsegmented negative RNA viruses, obligatory sequential transcription dictates that termination of each upstream gene is required for initiation of downstream genes.

Therefore, termination is a means of regulating expression of individual genes within the framework of a single transcriptional promoter. As will be seen, the mechanisms are dictated by the nature and structure of the viral genomes. The DNA polymerase involved must exhibit a high level of processivity and strand displacement characteristics. A duplex or r eplicative f orm RF results. Here, multiple cycles of continuous copying of a circular template, followed by discontinuous DNA synthesis on the displaced strand template produces linear dsDNA molecules containing multiple copies of the genome concatemers.

Rolling circle genome replication. Concatemeric DNA molecules are synthesized from a circular template by a rolling circle mechanism in which nicking of one strand allows the other to be copied continuously multiple times.

Discontinuous DNA synthesis on the displaced strand template produces linear dsDNA containing multiple copies of the genome. That is, the dsDNA molecules generated consist of head-to-tail linked genomes.

They are eventually cleaved at precise locations to release unit length genomes. Non-circular genomes may also replicate using an RC-like mechanism, that is, a variation of RCR named rolling-hairpin replication. ITRs are seen as terminal hairpin structures. These ITR regions interact with the viral-encoded Rep protein at specific binding sites to initiate replication using the host replication machinery.

Rep creates a nick between the hairpin and coding sequences. Refolding of the termini generates the same secondary structures present in the template DNA. The end result is a fully replicated viral genome with the same secondary structures.

This is the classical mode of replication used by eukaryotes and most nuclear dsDNA viruses, including the majority of phages. The step-wise assembly of replication initiation complexes at these ori sites then occurs followed by recruitment of topoisomerases that unwind dsDNA at each ori , and prevents supercoiling and torsional stress of the partially unwound template DNA. A replication fork or bubble is produced. Copying of the lagging strand requires discontinuous DNA synthesis that results in production of short DNA Okazaki fragments, which must then be ligated after the primers are removed by RNase H degradation.

Pararetroviruses e. Replication involves two phases; transcription of the pgRNA from virus DNA in the nucleus followed by reverse transcription in the cytoplasm. In contrast to retroviruses, virus DNA remains episomal and does not integrate into the host genome. Covalently closed virus dsDNA serves as a template for host polymerase transcription and the generation of viral pgRNA.

Upon transportation to the cytoplasm, capped and polyadenylated pgRNA is translated to viral proteins including the RT and is also used as template for subsequent reverse transcription catalyzed by virus RT.

The resulting dsDNA is either packaged into a new virion or targeted to the nucleus for another round of transcription. This mechanism pertains to all members of the family Retroviridae.

The process takes place in the cytoplasm, after viral entry. Only a small stretch of polypurines is resistant to degradation and this serves as a primer to initiate the synthesis of the cDNA. Integration is a key event in the replicative process of all retroviruses.

In some retroviruses, nuclear localization signals facilitate migration to the nucleus. Depending upon the retrovirus, preintegration complexes either enter the nuclei of nondividing cells through the n uclear p ore c omplex NPC e.

Moloney murine sarcoma virus, Murine leukemia virus ]. Once inside the nucleus and after association with host chromosomes, viral IN catalyzes insertion of viral sequences into the host DNA Fig. Integration of viral DNA e. A viral polyprotein is typically produced, which encodes the proteins required for replication. The replication process results in the formation of a dsRNA intermediate that is detected by the immune system.