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4.5: Viral Replication - Biology

4.5: Viral Replication - Biology


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4.5: Viral Replication

Viral replication is the formation of biological viruses during the infection process in the target host cells. Viruses must first enter the cell before viral replication can occur. Through the generation of abundant copies of its genome and the packaging of these copies, the virus continues to infect new hosts. The replication between viruses is very varied and depends on the type of genes involved in them. Most DNA viruses assemble in the nucleus, while most RNA viruses replicate only in the cytoplasm.

The virus does not have its own metabolic system. The infected host cell has to provide the energy, metabolic machinery and precursor molecules for the synthesis of viral proteins and nucleic acids.

Replication in viruses occurs in six steps which are named below.

  1. Adsorption/ attachment of the virus to host cell
  2. 2- Penetration of Viral components in the host cell
  3. Uncoating
  4. Synthesis of viral components by mRNA production / Transcription
  5. Virion assembly
  6. Release of virus (liberation stage)

1- Adsorption/ attachment of the virus to host cell

It is the first step of viral replication. The virus binds to the cell membrane of the host cell by a specific receptor site on the host cell membrane through binding proteins in the capsid or by glycoproteins embedded in the viral envelope. The specificity of this interaction determines the host (and the cells within the host) that can be infected by a particular virus. This can be imagined by thinking of multiple keys with multiple locks where each key will fit a single specific lock.

2- Penetration of Viral components in the host cell

Then the virus injects its DNA or RNA into the host to start the infection.

  • Bacteriophage nucleic acid enters the host cell naked, leaving the capsid outside the cell.
  • Plant and animal viruses can enter through endocytosis, in which the cell membrane surrounds and engulfs the entire virus. In the plant, the cell membrane of the host cell invaginates the virus particle, enclosing it in a pinocytotic vacuole.
  • Some enveloped viruses enter the cell when the viral envelope fuses directly with the cell membrane of the host cell.

3- Uncoating

Once inside the cell, the viral capsid is broken down by the cellular enzymes (from lysosomes) of the host and the viral nucleic acid is released, which is then available for replication and transcription.

4- Synthesis of viral components by mRNA production / Transcription

The virus uses cellular structures of the host cell to replicate. The replication mechanism depends on the viral genome.

  • DNA viruses generally use proteins and enzymes from the host cell to produce additional DNA that is transcribed into messenger RNA (mRNA), which is then used to direct protein synthesis.
  • RNA viruses generally use their RNA core as a template for the synthesis of viral genomic RNA (to be incorporated in the structure of new virus) and mRNA. Viral mRNA directs the host cell to synthesize two types of proteins.

a) Structural: The proteins that make up the viral particle are manufactured and assembled.
b) Non-structural: it is not found in viral particles. It is composed of enzymes for the replication of the virus genome.

If a host cell does not provide the enzymes necessary for viral replication, the viral genes provide the information to direct the synthesis of the missing proteins.

Retroviruses, like HIV, have an RNA genome that must be reverse transcribed into DNA, which is then incorporated into the host cell genome.

To convert RNA to DNA, retroviruses must contain genes that encode the enzyme reverse transcriptase for the virus-specific enzyme, which transcribes an RNA template into DNA.

The fact that HIV produces some of its own enzymes not found in the host has allowed researchers to develop drugs that inhibit these enzymes. These drugs, including the reverse transcriptase inhibitor AZT, inhibit HIV replication by reducing enzyme activity without affecting host metabolism. This approach has led to the development of a variety of drugs used to treat HIV and has been effective in reducing the amount of infectious virions (copies of viral RNA) in the blood to undetectable levels in many people infected with HIV.

A virion is simply an intact or active virus particle. At this stage, the newly synthesized genome (nucleic acid) and proteins assemble to form new virus particles.

This can take place in the cell nucleus, the cytoplasm, or in the plasma membrane of most developed viruses.

6- Release of virus (liberation stage)

It is the last stage of viral replication in which the viruses, which are now mature, are released in the host organism. They can then infect adjacent cells and repeat the replication cycle. Viruses are released by sudden cell disruption or by gradual extrusion (budding) of viruses enveloped through the cell membrane.

New viruses can invade or attack other cells, or remain dormant in the cell. In the case of bacterial viruses, the virions are released from the progeny by lysis of the infected bacteria. However, in the case of animal viruses, release generally occurs without cell lysis.


Abstract

Positive-strand RNA viruses are the largest genetic class of viruses and include many serious human pathogens. All positive-strand RNA viruses replicate their genomes in association with intracellular membrane rearrangements such as single- or double-membrane vesicles. However, the exact sites of RNA synthesis and crucial topological relationships between relevant membranes, vesicle interiors, surrounding lumens, and cytoplasm generally are poorly defined. We applied electron microscope tomography and complementary approaches to flock house virus (FHV)–infected Drosophila cells to provide the first 3-D analysis of such replication complexes. The sole FHV RNA replication factor, protein A, and FHV-specific 5-bromouridine 5'-triphosphate incorporation localized between inner and outer mitochondrial membranes inside ∼50-nm vesicles (spherules), which thus are FHV-induced compartments for viral RNA synthesis. All such FHV spherules were outer mitochondrial membrane invaginations with interiors connected to the cytoplasm by a necked channel of ∼10-nm diameter, which is sufficient for ribonucleotide import and product RNA export. Tomographic, biochemical, and other results imply that FHV spherules contain, on average, three RNA replication intermediates and an interior shell of ∼100 membrane-spanning, self-interacting protein As. The results identify spherules as the site of protein A and nascent RNA accumulation and define spherule topology, dimensions, and stoichiometry to reveal the nature and many details of the organization and function of the FHV RNA replication complex. The resulting insights appear relevant to many other positive-strand RNA viruses and support recently proposed structural and likely evolutionary parallels with retrovirus and double-stranded RNA virus virions.


SARS-CoV-2 Viral Replication in a High Throughput Human Primary Epithelial Airway Organ Model

COVID-19 emerged as a worldwide pandemic early in 2020, and at this writing has caused over 170 million cases and 3.7 million deaths worldwide, and almost 600,000 deaths in the United States. The rapid development of several safe and highly efficacious vaccines stands as one of the most extraordinary achievements in modern medicine, but the identification and administration of efficacious therapeutics to treat patients suffering from COVID-19 has been far less successful. A major factor limiting progress in the development of effective treatments has been a lack of suitable preclinical models for the disease, currently reliant upon various animal models and in vitro culture of immortalized cell lines. Here we report the first successful demonstration of SARS-CoV-2 infection and viral replication in a human primary cell-based organ-on-chip, leveraging a recently developed tissue culture platform known as PREDICT96. This successful demonstration of SARS-CoV-2 infection in human primary airway epithelial cells derived from a living donor represents a powerful new pathway for disease modeling and an avenue for screening therapeutic candidates in a high throughput platform.


Contents

Viruses multiply only in living cells. The host cell must provide the energy and synthetic machinery and the low molecular-weight precursors for the synthesis of viral proteins and nucleic acids. [2]

The virus replication occurs in seven stages, namely

  1. Attachment
  2. Entry,
  3. Uncoating, / mRNA production,
  4. Synthesis of virus components, assembly and
  5. Release (Liberation Stage).

Attachment Edit

It is the first step of viral replication. The virus attaches to the cell membrane of the host cell. It then injects its DNA or RNA into the host to initiate infection. In animal cells these viruses get into the cell through the process of endocytosis which works through fusing of the virus and fusing of the viral envelope with the cell membrane of the animal cell and in plant cells it enters through the process of pinocytosis which works on pinching of the viruses.

Entry Edit

The cell membrane of the host cell invaginates the virus particle, enclosing it in a pinocytotic vacuole. This protects the cell from antibodies like in the case of the HIV virus.

Uncoating Edit

Cell enzymes (from lysosomes) strip off the virus protein coat. This releases or renders accessible the virus nucleic acid or genome.

Transcription / mRNA production Edit

For some RNA viruses, the infecting RNA produces messenger RNA (mRNA). This is translation of the genome into protein products. For others with negative stranded RNA and DNA, viruses are produced by transcription then translation.

The mRNA is used to instruct the host cell to make virus components. The virus takes advantage of the existing cell structures to replicate itself.

Synthesis of virus components Edit

The following components are manufactured by the virus using the host's existing organelles:

  • Viral proteins: Viral mRNA is translated on cellular ribosomes into two types of viral protein:
    • Structural: proteins which make up the virus particle
    • Nonstructural: proteins not found in the virus particle, mainly enzymes for virus genome replication

    Virion assembly Edit

    A virion is simply an active or intact virus particle. In this stage, newly synthesized genome (nucleic acid), and proteins are assembled to form new virus particles.

    This may take place in the cell's nucleus, cytoplasm, or at plasma membrane for most developed viruses.

    Release (liberation stage) Edit

    The viruses, now being mature are released by either sudden rupture of the cell, or gradual extrusion (force out) of enveloped viruses through the cell membrane.

    The new viruses may invade or attack other cells, or remain dormant in the cell. In the case of bacterial viruses, the release of progeny virions takes place by lysis of the infected bacterium. However, in the case of animal viruses, release usually occurs without cell lysis.

    Viruses are classed into 7 types of genes, each of which has its own families of viruses, which in turn have differing replication strategies themselves. David Baltimore, a Nobel Prize-winning biologist, devised a system called the Baltimore Classification System to classify different viruses based on their unique replication strategy. There are seven different replication strategies based on this system (Baltimore Class I, II, III, IV, V, VI, VII). The seven classes of viruses are listed here briefly and in generalities. [3]

    Class 1: Double-stranded DNA viruses Edit

    This type of virus usually must enter the host nucleus before it is able to replicate. Some of these viruses require host cell polymerases to replicate their genome, while others, such as adenoviruses or herpes viruses, encode their own replication factors. However, in either cases, replication of the viral genome is highly dependent on a cellular state permissive to DNA replication and, thus, on the cell cycle. The virus may induce the cell to forcefully undergo cell division, which may lead to transformation of the cell and, ultimately, cancer. An example of a family within this classification is the Adenoviridae.

    There is only one well-studied example in which a class 1 family of viruses does not replicate within the nucleus. This is the Poxvirus family, which comprises highly pathogenic viruses that infect vertebrates.

    Class 2: Single-stranded DNA viruses Edit

    Viruses that fall under this category include ones that are not as well-studied, but still do pertain highly to vertebrates. Two examples include the Circoviridae and Parvoviridae. They replicate within the nucleus, and form a double-stranded DNA intermediate during replication. A human Anellovirus called TTV is included within this classification and is found in almost all humans, infecting them asymptomatically in nearly every major organ.

    Class 3: Double-stranded RNA viruses Edit

    Like most viruses with RNA genomes, double-stranded RNA viruses do not rely on host polymerases for replication to the extent that viruses with DNA genomes do. Double-stranded RNA viruses are not as well-studied as other classes. This class includes two major families, the Reoviridae and Birnaviridae. Replication is monocistronic and includes individual, segmented genomes, meaning that each of the genes codes for only one protein, unlike other viruses, which exhibit more complex translation.

    Classes 4 & 5: Single-stranded RNA viruses Edit

    These viruses consist of two types, however both share the fact that replication is primarily in the cytoplasm, and that replication is not as dependent on the cell cycle as that of DNA viruses. This class of viruses is also one of the most-studied types of viruses, alongside the double-stranded DNA viruses.

    Class 4: Single-stranded RNA viruses - positive-sense Edit

    The positive-sense RNA viruses and indeed all genes defined as positive-sense can be directly accessed by host ribosomes to immediately form proteins. These can be divided into two groups, both of which replicate in the cytoplasm:

    • Viruses with polycistronicmRNA where the genome RNA forms the mRNA and is translated into a polyprotein product that is subsequently cleaved to form the mature proteins. This means that the gene can utilize a few methods in which to produce proteins from the same strand of RNA, reducing the size of its genome.
    • Viruses with complex transcription, for which subgenomic mRNAs, ribosomal frameshifting and proteolytic processing of polyproteins may be used. All of which are different mechanisms with which to produce proteins from the same strand of RNA.

    Examples of this class include the families Coronaviridae, Flaviviridae, and Picornaviridae.

    Class 5: Single-stranded RNA viruses - negative-sense Edit

    The negative-sense RNA viruses and indeed all genes defined as negative-sense cannot be directly accessed by host ribosomes to immediately form proteins. Instead, they must be transcribed by viral polymerases into the "readable" complementary positive-sense. These can also be divided into two groups:

    • Viruses containing nonsegmented genomes for which the first step in replication is transcription from the negative-stranded genome by the viral RNA-dependent RNA polymerase to yield monocistronic mRNAs that code for the various viral proteins. A positive-sense genome copy that serves as template for production of the negative-strand genome is then produced. Replication is within the cytoplasm.
    • Viruses with segmented genomes for which replication occurs in the cytoplasm and for which the viral RNA-dependent RNA polymerase produces monocistronic mRNAs from each genome segment.

    Class 6: Positive-sense single-stranded RNA viruses that replicate through a DNA intermediate Edit

    A well-studied family of this class of viruses include the retroviruses. One defining feature is the use of reverse transcriptase to convert the positive-sense RNA into DNA. Instead of using the RNA for templates of proteins, they use DNA to create the templates, which is spliced into the host genome using integrase. Replication can then commence with the help of the host cell's polymerases.

    Class 7: Double-stranded DNA viruses that replicate through a single-stranded RNA intermediate Edit

    This small group of viruses, exemplified by the Hepatitis B virus, have a double-stranded, gapped genome that is subsequently filled in to form a covalently closed circle (cccDNA) that serves as a template for production of viral mRNAs and a subgenomic RNA. The pregenome RNA serves as template for the viral reverse transcriptase and for production of the DNA genome.


    How the dengue virus replicates in infected cells

    The nonstructural protein 1 (NS1) of the dengue virus interacts with another viral protein called NS4A-2K-4B to enable viral replication, according to a study published May 9 in the open-access journal PLOS Pathogens by Ralf Bartenschlager of the University of Heidelberg, and colleagues. As noted by the authors, the genetic map presented in the study offers a starting point for the design of antiviral agents targeting NS1, with the goal of suppressing viral replication as well as severe disease manifestations.

    Dengue virus is one of the most prevalent mosquito-transmitted human pathogens. Despite the serious socio-economic impact of dengue-associated diseases, the only licensed vaccine has limited efficacy and an antiviral therapy is not available. NS1 is secreted from infected cells, counteracts antiviral immune responses, and contributes to the severe clinical manifestations of dengue. In addition, NS1 is essential for the viral replication cycle, but the underlying molecular mechanism is unknown. To address this gap in knowledge, Bartenschlager and colleagues used a combination of genetic, biochemical and imaging approaches to determine the role of NS1 in the viral replication cycle.

    The researchers identified a cluster of amino acid residues in NS1 that is important for efficient secretion of this protein. Moreover, they identified a novel interaction between NS1 and the precursor of a viral protein called NS4A-2K-4B this interaction is required for viral RNA replication. The researchers also demonstrated that NS1 is required for the generation of the membranous dengue virus replication organelle in infected cells. This function does not require RNA replication and is independent from NS1's interaction with NS4A-2K-4B. Taken together, the results provide new insights into the role of NS1 in viral RNA replication and establish a genetic map of residues in NS1 required for the diverse functions of this protein.

    The authors add, "A detailed study of nonstructural protein 1 of Dengue virus identified determinants required for secretion of this protein, viral RNA replication and formation of the membranous replication organelle of this virus. A novel interaction of NS1 with a previously unrecognized NS4A-2K-NS4B precursor of the virus was found to be required for Dengue virus replication."


    Steps of Virus Infections

    Viral infection involves the incorporation of viral DNA into a host cell, replication of that material, and the release of the new viruses.

    Learning Objectives

    List the steps of viral replication and explain what occurs at each step

    Key Takeaways

    Key Points

    • Viral replication involves six steps: attachment, penetration, uncoating, replication, assembly, and release.
    • During attachment and penetration, the virus attaches itself to a host cell and injects its genetic material into it.
    • During uncoating, replication, and assembly, the viral DNA or RNA incorporates itself into the host cell’s genetic material and induces it to replicate the viral genome.
    • During release, the newly-created viruses are released from the host cell, either by causing the cell to break apart, waiting for the cell to die, or by budding off through the cell membrane.

    Key Terms

    • virion: a single individual particle of a virus (the viral equivalent of a cell)
    • glycoprotein: a protein with covalently-bonded carbohydrates
    • retrovirus: a virus that has a genome consisting of RNA

    Steps of Virus Infections

    A virus must use cell processes to replicate. The viral replication cycle can produce dramatic biochemical and structural changes in the host cell, which may cause cell damage. These changes, called cytopathic (causing cell damage) effects, can change cell functions or even destroy the cell. Some infected cells, such as those infected by the common cold virus known as rhinovirus, die through lysis (bursting) or apoptosis (programmed cell death or “cell suicide”), releasing all progeny virions at once. The symptoms of viral diseases result from the immune response to the virus, which attempts to control and eliminate the virus from the body and from cell damage caused by the virus. Many animal viruses, such as HIV (Human Immunodeficiency Virus), leave the infected cells of the immune system by a process known as budding, where virions leave the cell individually. During the budding process, the cell does not undergo lysis and is not immediately killed. However, the damage to the cells that the virus infects may make it impossible for the cells to function normally, even though the cells remain alive for a period of time. Most productive viral infections follow similar steps in the virus replication cycle: attachment, penetration, uncoating, replication, assembly, and release.

    Pathway to viral infection: In influenza virus infection, glycoproteins attach to a host epithelial cell. As a result, the virus is engulfed. RNA and proteins are made and assembled into new virions.

    Attachment

    A virus attaches to a specific receptor site on the host cell membrane through attachment proteins in the capsid or via glycoproteins embedded in the viral envelope. The specificity of this interaction determines the host (and the cells within the host) that can be infected by a particular virus. This can be illustrated by thinking of several keys and several locks where each key will fit only one specific lock.

    Entry

    The nucleic acid of bacteriophages enters the host cell naked, leaving the capsid outside the cell. Plant and animal viruses can enter through endocytosis, in which the cell membrane surrounds and engulfs the entire virus. Some enveloped viruses enter the cell when the viral envelope fuses directly with the cell membrane. Once inside the cell, the viral capsid is degraded and the viral nucleic acid is released, which then becomes available for replication and transcription.

    Replication and Assembly

    The replication mechanism depends on the viral genome. DNA viruses usually use host cell proteins and enzymes to make additional DNA that is transcribed to messenger RNA (mRNA), which is then used to direct protein synthesis. RNA viruses usually use the RNA core as a template for synthesis of viral genomic RNA and mRNA. The viral mRNA directs the host cell to synthesize viral enzymes and capsid proteins, and to assemble new virions. Of course, there are exceptions to this pattern. If a host cell does not provide the enzymes necessary for viral replication, viral genes supply the information to direct synthesis of the missing proteins. Retroviruses, such as HIV, have an RNA genome that must be reverse transcribed into DNA, which then is incorporated into the host cell genome.

    To convert RNA into DNA, retroviruses must contain genes that encode the virus-specific enzyme reverse transcriptase, which transcribes an RNA template to DNA. Reverse transcription never occurs in uninfected host cells the needed enzyme, reverse transcriptase, is only derived from the expression of viral genes within the infected host cells. The fact that HIV produces some of its own enzymes not found in the host has allowed researchers to develop drugs that inhibit these enzymes. These drugs, including the reverse transcriptase inhibitor AZT, inhibit HIV replication by reducing the activity of the enzyme without affecting the host’s metabolism. This approach has led to the development of a variety of drugs used to treat HIV and has been effective at reducing the number of infectious virions (copies of viral RNA) in the blood to non-detectable levels in many HIV-infected individuals.

    Egress

    The last stage of viral replication is the release of the new virions produced in the host organism. They are then able to infect adjacent cells and repeat the replication cycle. As you have learned, some viruses are released when the host cell dies, while other viruses can leave infected cells by budding through the membrane without directly killing the cell.


    Viral Replication

    Viruses (virions) have to make more copies of themselves so they can spread. This is what we call viral replication.

    In general, virus replication goes through the following five steps:
    1. Adsorption, the attachment of viruses to host cells.

    Penetration, the entry of virions (or their genome) into host cells. Some leave the capsid and envelope behind.

    Synthesis, the synthesis of new nucleic acid molecules, capsid proteins, and other viral components within host cells while using the metabolic machinery of those cells. They hijack the cells' metabolic processes.

    Maturation, the assembly of newly synthesized viral components into complete virions.

    Release, the departure of new virions from host cells. Release generally, but not always, kills (lyses) host cells. (Some types will wait for a long time while hiding and are said to be lysogenic).


    Researchers identify potential new antiviral drug for COVID-19

    The experimental drug TEMPOL may be a promising oral antiviral treatment for COVID-19, suggests a study of cell cultures by researchers at the National Institutes of Health. TEMPOL can limit SARS-CoV-2 infection by impairing the activity of a viral enzyme called RNA replicase. The work was led by researchers at NIH's Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD). The study appears in Science.

    "We urgently need additional effective, accessible treatments for COVID-19," said Diana W. Bianchi, M.D., NICHD Director. "An oral drug that prevents SARS-CoV-2 from replicating would be an important tool for reducing the severity of the disease."

    The study team was led by Tracey A. Rouault, M.D., head of the NICHD Section on Human Iron Metabolism. It discovered TEMPOL's effectiveness by evaluating a more basic question on how the virus uses its RNA replicase, an enzyme that allows SARS-CoV-2 to replicate its genome and make copies of itself once inside a cell.

    Researchers tested whether the RNA replicase (specifically the enzyme's nsp12 subunit) requires iron-sulfur clusters for structural support. Their findings indicate that the SARS-CoV-2 RNA replicase requires two iron-sulfur clusters to function optimally. Earlier studies had mistakenly identified these iron-sulfur cluster binding sites for zinc-binding sites, likely because iron-sulfur clusters degrade easily under standard experimental conditions.

    Identifying this characteristic of the RNA replicase also enables researchers to exploit a weakness in the virus. TEMPOL can degrade iron-sulfur clusters, and previous research from the Rouault Lab has shown the drug may be effective in other diseases that involve iron-sulfur clusters. In cell culture experiments with live SARS-CoV-2 virus, the study team found that the drug can inhibit viral replication.

    Based on previous animal studies of TEMPOL in other diseases, the study authors noted that the TEMPOL doses used in their antiviral experiments could likely be achieved in tissues that are primary targets for the virus, such as the salivary glands and the lungs.

    "Given TEMPOL's safety profile and the dosage considered therapeutic in our study, we are hopeful," said Dr. Rouault. "However, clinical studies are needed to determine if the drug is effective in patients, particularly early in the disease course when the virus begins to replicate."

    The study team plans on conducting additional animal studies and will seek opportunities to evaluate TEMPOL in a clinical study of COVID-19.

    NIH authors on the study include researchers from the National Cancer Institute, the National Institute of Allergy and Infectious Diseases, and the National Institute of Neurological Disorders and Stroke. Authors from the Pennsylvania State University are funded by NIH's National Institute of General Medical Sciences.


    The first 150 to 200 nucleotides within the 5′ UTR of Alphacoronaviruses are highly structured and shown to be conserved on the structural level. The 5′ UTRs are predicted to contain three conserved stem-loops: [3]

    • SL1 is important for viral replication, most likely playing a role in the template-switch of viral subgenomic RNA (sgRNA) transcription. Mutations of the upper part of SL1 seem to have a higher impact of viral replication level.
    • SL2 is crucial for viral viability. Nucleotides are interchangeable as long as the structure remains stable. Disrupting any G-C pairing causes major defects in viral replication.
    • SL4 is hypothesised to play a role in directing subgenomic RNA synthesis during viral replication.

    Downstream of SL4 lies SL5, which overlaps with the first ORF of the viral genome. The three terminal loops of SL5 contain a conserved sequence 5′-UUCCGU-3′ and are thought to act as the packaging signal. [2]

    Similar to Alphacoronavirus, the first 150 to 200 nucleotides within the Betacoronavirus 5′ UTR are highly structured and contains three conserved stem-loops (SL1, SL2 and SL4).

    SARS-CoV and BCoV have an additional stem-loop, called SL3, which contains the TRS-L sequence in its loop region. [4] This is crucial for sgRNA synthesis during viral replication. However, according to predictions, SL3 is not stable in other Betacoronaviruses like MHV.

    Similar to other Sarbecoviruses, the 5′ UTR of SARS-CoV-2 is predicted to consist of 4 distinct stem-loops, namely SL1, SL2, SL3 and SL4. Further, there is a larger structure, SL5, present, which includes the first ORFs of the polyprotein pp1a. Note, that SL3 is typically present in SARS coronaviruses, but not necessarily conserved among other Betacoronaviruses. [5]

    The 5′ UTR of Gammacoronaviruses is similar to the 5′ UTRs of Alpha- and Betacoronaviruses, as they also contain three helices denoted as SL1, SL2 and SL4. Further, in a subset of Gammacoronaviruses a third stem-loop, SL3, is observed. SL1 and SL2 have major impacts of the level of viral replication, whereas SL4 is hypothesized to play a role as a "spacer" during the template-switch of sgRNA synthesis.

    The 5′UTR of Deltacoronaviruses is similar to the 5′UTRs of Alpha- and Betacoronaviruses, as they also contain three helices denoted as SL1, SL2 and SL4. Predictions show a conserved fourth stem-loop (SL3) between SL2 and SL4, sometimes observed in Beta- and Gammacoronaviruses as well. SL3 usually exposes the TRS-L sequence in the loop region.


    Watch the video: HIV VIRUS REPLICATION 3D (June 2022).


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