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A Primer on Coronavirus, Variants, Mutation and Evolution. SARS-CoV-2 is an RNA virus that has an inherently high mutation rate. Mechanisms of Retroviral Recombination The exact mechanism by which two retroviral RNA genome strands are copackaged into a single virionmatingis only partially understood. Prompted by the hypothesis that their earliest progenitors recruited host proteins for virion formation, we have used stringent laboratory evolution to convert a bacterial enzyme that lacks affinity for nucleic acids into an artificial nucleocapsid that efficiently packages and protects multiple copies of its own encoding messenger RNA. RNA viruses mutate faster than DNA viruses, single-stranded viruses mutate faster than double-strand virus, and genome size appears to correlate negatively with mutation rate. Viruses are little more than parasitic fragments of RNA or DNA. The S protein mediates Although ribavirin was discovered in 1972, its mechanism of action has remained unclear until recently. The below is an interview with Rob Dunn (RRD), Matt Koci (MK), Sergios-Orestis Kolokotronis (SOK), David Rasmussen (DAR), and Jessica Brinkworth (JFB). For example, flu strains can arise this way. Errors made by the RNA-dependent RNA-polymerase (RdRP) viral replicase are a 25 source of mutations, however in coronaviruses some of these errors can be corrected by a 26 proofreading RNA exonuclease ExoN [3, 4]. Viral mutation rates are modulated at different levels, including polymerase fidelity, sequence context, template secondary structure, cellular microenvironment, replication mechanisms, proofreading, and access to post If the organism has a conservative replication mechanism, as is the case for RNA viruses, then mutations would occur, with certain probabilities, only in the descendant copy, while the parent copy would remain unchanged (that may also be the case in organisms with double-stranded genomes, where the methylation mechanism keeps a master copy of the genome preserved). Viruses undergo evolution and natural selection, just like cell-based life, and most of them evolve rapidly. One of the best-studied systems for RNA virus mutation is poliovirus, in which a now frequently used lower mutation rate mutant (G64S in the 3D RNA-dependent RNA polymerase, 3D:G64S) was characterized, simultaneously, by virologists working at two locations in the San Francisco Bay Area [17, 18]. A virus is a submicroscopic infectious agent that replicates only inside the living cells of an organism. Sex recreates mutation-free genotypes and helps to keep the average population fitness high (Otto & Lenormand, 2002). Together with Abstract. In positive-sense RNA virus transcription, unlike in negative-sense RNA virus transcription or DNA-dependent transcription, the template:nascent RNA duplex is likely to extend a considerable distance behind the RdRp footprint, possibly only being disassociated when the next RdRp passes along the template 39 40 41. Viruses do not form fossils in the traditional sense, because they are much smaller than the finest colloidal fragments forming sedimentary rocks that fossilize plants and animals. Viruses are ubiquitous pathogens of global impact. However, RNA viruses experience high mutation rates, and the proportion of genomes with lethal mutations increases with the number of replication cycles. After the protein piece is made, the cell breaks down the instructions and gets rid of them. Unraveling the exact molecular mechanism(s) for these results would be of great interest. These mutations drive viral evolution and genome variability, thereby facilitating viruses to have rapid antigenic shifting to evade host immunity The easiest way for these deleterious mutations to reach high frequency is their linkage with a beneficial mutation. Thus, RNA viruses would greatly benefit from evolving recombination mechanisms to purge these deleterious mutations, while consolidating beneficial ones. Despite this, they are astonishingly abundant in number and genetic diversity. RNA viruses mutate faster than DNA viruses, single-stranded viruses mutate faster than double-strand virus, and genome size appears to correlate negatively with mutation rate. Like all living things, influenza makes small errorsmutationswhen it copies its genetic code during reproduction. Strand switching during RdRp copying is also a mechanism for RNA recombination, allowing RNA viruses to repair deleterious mutations, rearrange genes, and acquire new genes from other viruses or their hosts . RNA viruses can be further classified according to the sense or polarity of their RNA into negative-sense and positive-sense, or ambisense RNA viruses. All viruses are either RNA viruses or DNA viruses. (viii) Finally, RNA viruses show extremely high mutation rates (2). However, large population size, complementation, cellular chaperones, and recombination can buffer viral populations against deleterious and lethal mutations. The single most important feature of RNA viruses is their high mutation rate. They rapidly adapt to environmental changes, such as shifts in immune pressure or pharmacological challenge. Nonsense-mediated mRNA decay protects us from many genetic mutations that could cause disease if NMD werenot active to destroy the RNA harboring the mutation, she says. This mechanism accelerates, and directs, adaptation: While introduction of lethal mutations to most RNA genomes may not adversely influence quasispecies, replicative homeostasis ensures any RNA mutations that do arise, and that result in beneficial phenotype(s), will favour replication of that RNA molecule, ensuring that phenotype is retained within the quasispecies. Several viruses, in particular RNA viruses, have high mutation rates and relatively short generation times. However, the genomes of many organisms contain endogenous viral elements (EVEs). The complete virus requires all four of these proteins to be present. In general, RNA viruses dont have a proofreading mechanism, whereas DNA viruses do. So when an RNA virus replicates, its much more likely to have mistakes called mutations. Investigations of immune evasion mechanisms developed by RNA viruses will help to understand the pathogenesis of viral infection and discover novel therapeutic targets for prevention and treatment of the diseases. The RNA-synthesizing machinery that most RNA viruses use to copy their genome doesnt have this error correction mechanism. The structural proteins include the spike (S) protein, the nucleocapsid (N) protein, the envelope (E) protein, and the membrane (M) protein. So when an RNA virus replicates, its much more likely to have mistakes called mutations. Negative-sense viral RNA is complementary to mRNA and thus must be converted to positive-sense RNA by an RNA-dependent RNA polymerasebefore translation. It is a single-stranded RNA virus whose complex metabolism remains comparable to RNA viruses such as Influenza virus, some hemorrhagic fever viruses (such as Ebola virus or Hantavirus), Human Immunodeficiency Virus (HIV) and Coxsac Before the influenza A/H1N1 pandemic in 2009, most human influenza A/H1N1 viruses contained the avian-associated residue, serine, at position 216 in PB1. SARS-CoV-2 is responsible for the COVID-19 pandemic that started in Wuhan, Hubei province, China and which already claimed more than 340,000 lives worldwide as of May 23, 2020 (1). One of the weapons in our cells arsenal is an RNA surveillance mechanism Maquat discovered called nonsense-mediated mRNA decay (NMD). Viruses infect all life forms, from animals and plants to microorganisms, including bacteria and archaea. In contrast to our assumption that most polymorphic mutations are beneficial, there are some studies showing that in natural populations of RNA viruses many high frequency mutations are deleterious, and will be later purged by natural selection . This mechanism does not alter the amplitude of the mutant spectrum, and the corresponding adaptive flexibility. RNA viruses mutate faster than DNA viruses, single-stranded viruses mutate faster than double-strand virus, and genome size appears to correlate negatively with mutation rate. The replication strategy that maximizes the intracellular growth rate of the virus requires iterative genome transcription from positive to negative, and back to positive sense. One way to limit cell death is by generating and accumulating defective genomes. In general, RNA viruses dont have a proofreading mechanism, whereas DNA viruses do. RNA viruses are characterized by extreme mutation rates that are orders of magnitudes higher than those of most DNA-based organisms 1, 2. Once the instructions (mRNA) are inside the immune cells, the cells use them to make the protein piece. RNA viruses are excellent candidates for genetic degeneration because they typically have an extraordinarily high mutation rate [14]. RNA viruses are unique in their evolutionary capacity, exhibiting high mutation rates and frequent recombination. The frequency of mutant genomes increase and Viral mutation rates are modulated at different levels, including polymerase fidelity, sequence context, template secondary structure, cellular microenvironment, replication mechanisms, proofreading, and access to Lucie Ciccone graciously lent their insights and served as additional sets of eyes. Most of the well-studied mechanisms of persistence of RNA viruses in primary cell cultures or established cell lines involve genetic variation of the virus, the cell, or both. As a result, influenza is not genetically stable. Using poliovirus as an RNA virus model, it was shown that ribavirin is a virus mutagen, and it was proposed that the primary mechanism of action of ribavirin is via lethal mutagenesis The rapid development of the SARS-CoV-2 mediated COVID-19 pandemic has been the cause of significant health concern, highlighting the immediate need for effective antivirals. I dont think it works quite as well as the DNA mechanism, though. The spike protein is found on the surface of the virus that causes COVID-19. Mutations in the PB1 subunit of RNA-dependent RNA polymerase (RdRp) of influenza A virus can affect replication fidelity. found that D614G mutation increases the infectivity of SARS-CoV-2. The high mutation rate of RNA viruses is postulated to be an adaptation for evolvability3,4, but the paradox is that whereas some RNA viruses evolve at high rates4,5, others are highly stable5,6. Positive-sense viral RNA is similar to mRNA and thus can be immediately translated by the host cell. These In this study, we investigated the determinants of the equilibrium frequency of potential colonists in the RNA bacteriophage 6. These DNA sequences are the remnants of ancient virus genes and genomes that ancestrally 'invaded' the host germline. In the RNA virus world, RNA-dependent RNA polymerases (RdRps) lack co- and postreplicative fidelity-enhancing pathways, and final RNA genome copies incorporate mutations at a much higher rate than that observed for DNA genomes (1). A mutation that speeds up COVID-19's spread might explain why the virusknown as SARS-CoV-2has so rapidly moved through North America and Europe, where the G614 mutated version is predominant. The ability of a virus population to colonize a novel host is predicted to depend on the equilibrium frequency of potential colonists ( i.e ., genotypes capable of infecting the novel host) in the source population. Without the capacity to detect and repair mismatched or damaged nucleotides, viral RNA genomes are prone to mutations introduced by mechanisms intrinsic and extrinsic to viral replication. Genome comparisons imply that such RNA recombination has been the major force in RNA virus evolution. Because of the lack of proofreading by their replicases, RNA viruses show the highest mutation rates among living beings (2), on the order of one mutation per genome and replication round. apolipoprotein B mRNA editing catalytic polypeptide-like and But coronaviruses have a special enzyme that allows them to do error correction, so they have a lower mutation rate than other RNA viruses. We don't know how many virus For example, the genomes of most vertebrate species contain hundreds to thousands of sequences derived from ancient retroviruses. The 3D:G64S strains not only have a lower mutation rate than wild-type polio but also are 23 quasispecies - populations of viruses differing in several genomic positions from the original 24 virus [2]. Purified RNA of a positive-sense virus can directly cause infection though it may be less infectious tha However, near the onset of the 2009 pandemic, human viruses began to acquire the mammalian-associated residue, While some mutations are beneficial, the accumulation of deleterious mutations leads to virus attenuation [52]. But influenza lacks the ability to repair those errors, because it is an RNA virus; RNA, unlike DNA, lacks a self-correcting mechanism. Strand switching during RdRp copying is also a mechanism for RNA recombination, allowing RNA viruses to repair deleterious mutations, rearrange genes, and acquire new genes from other viruses or their hosts ( 17 ). Genome comparisons imply that such RNA recombination has been the major force in RNA virus evolution. Viral mutation rates are modulated at different levels, including polymerase fidelity, sequence context, template secondary structure, cellular microenvironment, replication mechanisms, proofreading, and access to The higher mutation rate of RNA viruses is a consequence of the novel mechanisms required for RNA replication, which are especially prone to mutation, and the lack of ef fective repair enzymes for RNA replication. RNA viruses readily mutate, and genomes can accumulate mutations to high levels. First, COVID-19 mRNA vaccines are given in the upper arm muscle. In turn, the data suggest that evolution of mutational robustness (whatever the underlying molecular mechanism) allows RNA viruses to tolerate less-accurate genome replication, perhaps explaining why these viruses remain highly mutable. Recently, Korber et al. The mutation rate of RNA viruses. Another population robustness mechanism that might be important for RNA viruses is sex, as it results in not only recombination between homologous molecules, but also the segregation of segments in a multipartite genome.