This process is repeated over and over: the viruses advance through the body killing cells. The body activates the immune system to combat them and keep them from continuing to do damage. Understanding the life cycle of viruses allows you to think of the best way to protect yourself from them.
It's easy to confuse viruses and bacteria. However, there are several differences between the two. Do you know what they are? Health Illnesses. The Reproductive Cycle of Viruses 4 minutes. The reproductive cycle of viruses is a process in which they use a living being to multiply. Once viruses multiply, they damage the same organism to free themselves and multiply in another body. The Differences Between Viruses and Bacteria. Gomez-Lucia, E. 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. Depending on the virus, sgRNAs may be generated during internal initiation on a minus-strand RNA template and require an internal promoter or there is the generation of a prematurely terminated minus-strand RNA that is used as template to make the sgRNAs.
The resulting chimeric sg minus-strand RNA can in turn function as a template for the production of subgenomic positive-strand RNAs. Translation of this mRNA generates proteins required for replication and viral encapsidation. As such, many dsRNA viruses undergo replication within their icosahedral capsids.
The replicating RNA polymerases are located within the capsid and produce mRNA strands that are extruded from the particle. Replication occurs in the cytoplasm. The viral RdRP complex is assumed to be the same for both replication and transcription and can switch off functions as required. Of note, two genome subgroups can be distinguished in this group: nonsegmented and segmented.
Viruses with segmented genomes replicate in the nucleus, and the RdRp produces one monocistronic mRNA strand from each genome segment. The mode of transcription is similar to eukaryotic transcriptional events in which the process is divided into three steps: 1 the initiation step, when a transcription initiation complex is assembled at the promoter region located upstream of the transcriptional start site, allowing for the recruitment of the RNA polymerase, 2 the elongation step, in which, the polymerase is recruited to template DNA, is activated by phosphorylation of the c arboxy- t erminal d omain CTD , and proceeds to transcribe the template DNA to RNA, and 3 the termination step, which involves the recognition of specific signals, including the polyadenylation signal.
For productive infection, viruses must then utilize this machinery, and remain both stable and undetected in the cell. Furthermore, while the great majority of cellular mRNAs are monocistronic, viruses must often express multiple proteins from their mRNAs.
As a result, viruses have evolved a number of mechanisms to allow translation to be customized to their specific needs. Straightforward exploitation of the cellular capping machinery is typical of DNA viruses that replicate in the nucleus. Other strategies used by viruses include internal initiation of translation of uncapped RNAs in picornaviruses and their relatives, snatching of capped oligonucleotides from host pre-mRNAs to initiate viral transcription in segmented negative-strand RNA viruses, and recruitment of genes for the conventional, eukaryotic-type capping enzymes that apparently occurred independently in diverse groups of viruses flaviviruses, reoviridae, poxviruses, asfarviruses, some iridoviruses, phycodnaviruses, mimiviruses, baculoviruses, nudiviruses.
For instance, flaviviruses e. Other examples that follow the same strategy include rotaviruses, barley yellow dwarf viruses, and possibly Hepacivirus C HCV. Since eukaryotic cells are not equipped to translate polycistronic mRNA into several individual proteins, DNA viruses overcome this limitation by using the cellular mechanism of splicing of their polycistronic mRNA to monocistronic mRNA. RNA viruses, on the other hand, that mostly replicate in the cytoplasm, do not have access to these host mechanisms and consequently produce monocistronic sgRNAs e.
However, the use of these mechanisms is not without consequences: 1 some viral proteins may be expressed from sgRNAs but the components of the replication complex that are needed early in infection must still be translated from the genomic RNA, 2 viruses with segmented genomes have to ensure the correct packaging of the different segments, and 3 polyprotein expression represents an inefficient use of host cell resources as all virus proteins are produced in equal amounts, even though catalytic proteins are often required in much smaller quantities than the structural proteins.
Alternative and more efficient mechanisms of expressing multiple proteins from a single viral mRNA involve internal ribosome entry, leaky scanning, ribosome shunting, reinitiation, ribosomal frameshifting, and stop codon read-through.
Viral gene expression is facilitated by the possession of regulatory signals within viral mRNAs that are recognizable by the host cell.
These signals ultimately enable the virus to shut off host gene expression to ensure preferential viral gene expression. The strategies are reviewed in the section that follows. Transcription can be viewed as a highly regulated 3-phase process: initiation, elongation, and termination. Initiation of transcription requires the recruitment and assembly of a large multiprotein DNA-binding transcription initiation complex. During the course of evolution, several viruses have developed strategies that affect the loading of host transcription initiation factors into transcription complexes, which ultimately shuts down host protein synthesis Fig.
Pathogenic Yersiniae. Immune responses to viruses. Intestinal nematode parasites: mechanisms of resistance. Immune responses to fungal pathogens. Immune responses to bacteria. Chlamydia Trachomatis. Candida albicans. Aspergillus fumigatus. Chronic Obstructive Pulmonary Disease. By Regina Bailey Regina Bailey. Regina Bailey is a board-certified registered nurse, science writer and educator.
Learn about our Editorial Process. How Viruses Infect Cells The basic process of viral infection and virus replication occurs in 6 main steps. Adsorption - virus binds to the host cell. Penetration - virus injects its genome into host cell. Viral Genome Replication - viral genome replicates using the host's cellular machinery.
Assembly - viral components and enzymes are produced and begin to assemble. Maturation - viral components assemble and viruses fully develop. Release - newly produced viruses are expelled from the host cell. Featured Video. Cite this Article Format. Bailey, Regina. Learn How Virus Replication Occurs. Differences Between Bacteria and Viruses.
0コメント