Viral replication in the context of Genetic mutations


Viral replication in the context of Genetic mutations

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⭐ Core Definition: Viral replication

Viral replication is the formation of biological viruses during the infection process in the target host cells. Viruses must first get into the cell before viral replication can occur. Through the generation of abundant copies of its genome and packaging these copies, the virus continues infecting new hosts. Replication between viruses is greatly varied and depends on the type of genes involved in them. Most DNA viruses assemble in the nucleus while most RNA viruses develop solely in cytoplasm.

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Viral replication in the context of Self-replication

Self-replication is any behavior of a dynamical system that yields construction of an identical or similar copy of itself. Biological cells, given suitable environments, reproduce by cell division. During cell division, DNA is replicated and can be transmitted to offspring during reproduction. Biological viruses can replicate, but only by commandeering the reproductive machinery of cells through a process of infection. Harmful prion proteins can replicate by converting normal proteins into rogue forms. Computer viruses reproduce using the hardware and software already present on computers. Self-replication in robotics has been an area of research and a subject of interest in science fiction. Any self-replicating mechanism which does not make a perfect copy (mutation) will experience genetic variation and will create variants of itself. These variants will be subject to natural selection, since some will be better at surviving in their current environment than others and will out-breed them.

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Viral replication in the context of Mutation

In biology, a mutation is an alteration in the nucleic acid sequence of the genome of an organism, virus, or extrachromosomal DNA. Viral genomes contain either DNA or RNA. Mutations result from errors during DNA or viral replication, mitosis, or meiosis or other types of damage to DNA (such as pyrimidine dimers caused by exposure to ultraviolet radiation), which then may undergo error-prone repair (especially microhomology-mediated end joining), cause an error during other forms of repair, or cause an error during replication (translesion synthesis). Mutations may also result from substitution, insertion or deletion of segments of DNA due to mobile genetic elements.

Mutations may or may not produce detectable changes in the observable characteristics (phenotype) of an organism. Mutations play a part in both normal and abnormal biological processes including: evolution, cancer, and the development of the immune system, including junctional diversity. Mutation is the ultimate source of all genetic variation, providing the raw material on which evolutionary forces such as natural selection can act.

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Viral replication in the context of Baltimore classification

Baltimore classification is a system used to classify viruses by their routes of transferring genetic information from the genome to messenger RNA (mRNA). Seven Baltimore groups, or classes, exist and are numbered in Roman numerals from I to VII. Groups are defined by whether the viral genome is made of deoxyribonucleic acid (DNA) or ribonucleic acid (RNA), whether the genome is single- or double-stranded, whether a single-stranded RNA genome is positive-sense (+) or negative-sense (–), and whether the virus makes DNA from RNA (reverse transcription (RT)). Viruses within Baltimore groups typically have the same replication method, but other characteristics such as virion structure are not directly related to Baltimore classification.

The seven Baltimore groups are for double-stranded DNA (dsDNA) viruses, single-stranded DNA (ssDNA) viruses, double-stranded RNA (dsRNA) viruses, positive-sense single-stranded RNA (+ssRNA) viruses, negative-sense single-stranded RNA (–ssRNA) viruses, ssRNA viruses that have a DNA intermediate in their life cycle (ssRNA-RT), and dsDNA viruses that have an RNA intermediate in their life cycle (dsDNA-RT). Only one class exists for ssDNA viruses because their genomes are converted to dsDNA before transcription regardless of sense. Some viruses belong to more than one Baltimore group, such as DNA viruses that have either dsDNA or ssDNA as their genome.

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Viral replication in the context of Ribozyme

Ribozymes (ribonucleic acid enzymes) are RNA molecules that have the ability to catalyze specific biochemical reactions, including RNA splicing in gene expression, similar to the action of protein enzymes. The 1982 discovery of ribozymes demonstrated that RNA can be both genetic material (like DNA) and a biological catalyst (like proteins), and contributed to the RNA world hypothesis, which suggests that RNA may have been important in the evolution of prebiotic self-replicating systems.

The most common activities of natural or in vitro evolved ribozymes are the cleavage or ligation of RNA and DNA, and peptide bond formation. For example, the smallest ribozyme known (GUGGC-3') can aminoacylate a GCCU-3' sequence in the presence of Phenylalanyl-Adenosine Monophosphate. Within the ribosome, ribozymes function as part of the large subunit ribosomal RNA to link amino acids during protein synthesis. They also participate in a variety of RNA processing reactions, including RNA splicing, viral replication, and transfer RNA biosynthesis. Examples of ribozymes include the hammerhead ribozyme, the VS ribozyme, leadzyme, and the hairpin ribozyme.

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Viral replication in the context of Antibody-dependent enhancement

Antibody-dependent enhancement (ADE), sometimes less precisely called immune enhancement or disease enhancement, is a phenomenon in which binding of a virus to suboptimal antibodies enhances its entry into host cells, followed by its replication. The suboptimal antibodies can result from natural infection or from vaccination. ADE may cause enhanced respiratory disease, but is not limited to respiratory disease. It has been observed in HIV, RSV, and Dengue virus and is monitored for in vaccine development.

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Viral replication in the context of Riboviria

Riboviria is a realm of viruses that includes all viruses that use a homologous RNA-dependent polymerase for replication. It includes RNA viruses that encode an RNA-dependent RNA polymerase, as well as reverse-transcribing viruses (with either RNA or DNA genomes) that encode an RNA-dependent DNA polymerase. RNA-dependent RNA polymerase (RdRp), also called RNA replicase, produces RNA (ribonucleic acid) from RNA. RNA-dependent DNA polymerase (RdDp), also called reverse transcriptase (RT), produces DNA (deoxyribonucleic acid) from RNA. These enzymes are essential for replicating the viral genome and transcribing viral genes into messenger RNA (mRNA) for translation of viral proteins.

Riboviria was established in 2018 to accommodate all RdRp-encoding RNA viruses and was expanded a year later to also include RdDp-encoding viruses. These two groups of viruses are assigned to two separate kingdoms: Orthornavirae for RdRp-encoding RNA viruses, and Pararnavirae for RdDp-encoding viruses, i.e. all reverse-transcribing viruses. Most identified eukaryotic viruses belong to the realm, including most human, animal, and plant viruses. Historically, few prokaryotic RNA viruses had been discovered to be included in the realm, but in the 2020s metagenomic and metatranscriptomic studies have discovered many prokaryotic RNA viruses.

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