In The Lysogenic Cycle _____.

Procedure of virus reproduction

Lysogenic cycle, compared to lytic wheel

Lysogenic Cycle:1. The prokaryotic cell is shown with its Dna, in greenish. 2. The bacteriophage attaches and releases its Dna, shown in cherry, into the prokaryotic cell. three. The phage DNA then moves through the cell to the host's DNA. 4. The phage Deoxyribonucleic acid integrates itself into the host cell's DNA, creating prophage. 5. The prophage then remains fallow until the host cell divides. 6. Subsequently the host cell has divided, the phage Dna in the daughter cells activate, and the phage Deoxyribonucleic acid begins to express itself. Some of the cells containing the prophage get on to create new phages which will movement on to infect other cells.

Lysogeny, or the lysogenic cycle, is i of two cycles of viral reproduction (the lytic bike being the other). Lysogeny is characterized by integration of the bacteriophage nucleic acid into the host bacterium's genome or formation of a circular replicon in the bacterial cytoplasm. In this condition the bacterium continues to live and reproduce normally, while the bacteriophage lies in a dormant state in the host jail cell. The genetic material of the bacteriophage, called a prophage, can be transmitted to daughter cells at each subsequent cell division, and later events (such as UV radiation or the presence of certain chemicals) can release it, causing proliferation of new phages via the lytic cycle.^[1] Lysogenic cycles can also occur in eukaryotes, although the method of Deoxyribonucleic acid incorporation is not fully understood. For instance the AIDS viruses can either infect humans (or some other primates) lytically, or lay dormant (lysogenic) as role of the infected cells' genome, keeping the power to render to lysis at a later on time. The rest of this article is about lysogeny in bacterial hosts.

The difference betwixt lysogenic and lytic cycles is that, in lysogenic cycles, the spread of the viral Dna occurs through the usual prokaryotic reproduction, whereas a lytic wheel is more immediate in that it results in many copies of the virus being created very quickly and the cell is destroyed. One central deviation between the lytic cycle and the lysogenic cycle is that the latter does not lyse the host jail cell directly abroad.^[2] Phages that replicate simply via the lytic bike are known as virulent phages while phages that replicate using both lytic and lysogenic cycles are known as temperate phages.^[ane]

In the lysogenic cycle, the phage Dna first integrates into the bacterial chromosome to produce the prophage. When the bacterium reproduces, the prophage is also copied and is present in each of the daughter cells. The daughter cells can continue to replicate with the prophage present or the prophage can get out the bacterial chromosome to initiate the lytic cycle.^[1] In the lysogenic cycle the host Dna is not hydrolyzed but in the lytic bicycle the host Deoxyribonucleic acid is hydrolyzed in the lytic phase.

Bacteriophages [edit]

Bacteriophages are viruses that infect and replicate inside a bacterium. Temperate phages (such as lambda phage) can reproduce using both the lytic and the lysogenic cycle.^{[ citation needed ]}

How a phage decides which wheel to enter depends on a variety of factors.^[3] For case, if in that location are several other infecting phages (or if there is a loftier multiplicity), information technology is probable that the phage will utilise the lysogenic wheel. This may exist useful in helping reduce the overall phage-to-host ratio and therefore preventing the phages from killing their hosts, also thereby increasing the phage's potential for survival, making this a form of natural selection. A phage may decide to exit the chromosome and enter the lytic bike if it is exposed to Deoxyribonucleic acid-damaging agents, such equally UV radiation and chemicals. Other factors with the potential to induce temperate phage release include temperature, pH, osmotic pressure, and low food concentration.^[iv] Still, phages may also re-enter the lytic cycle spontaneously. In eighty-ninety% of single-prison cell infections, phages enter the lysogenic cycle. In the other 10-20%, phages enter the lytic wheel.^{[ citation needed ]}

Testify of Lysogeny [edit]

Information technology is sometimes possible to find which wheel a phage enters past looking at the plaque morphology in bacterial plate culture.^[five] Since phages that enter the lytic bicycle kill the host bacterial cells, plaques volition appear clear (photo A). The plaques may besides appear to take a halo-like ring effectually the edge, indicating that these cells were not fully lysed. In dissimilarity, infecting phages that enter the lysogenic cycle volition produce cloudy or turbid plaques, as the cells containing the lysogenic phage are not lysed and can continue growing (photo B). However, exceptions to this dominion are as well known to exist, where non-temperate phages withal showroom cloudy plaques, and temperate phage mutants can generate clear plaques equally a issue of loss of lysogen formation ability.^{[ commendation needed ]}

Encounter a comparing of clear and turbid plaques, formed by lytic and lysogenic phages, respectively, in the Phage Discovery Guide.

Detection methods of phages released from the lysogenic cycle include electron microscopy, Deoxyribonucleic acid extraction, or propagation on sensitive strains.^[half-dozen]

Via the lysogenic cycle, the bacteriophage'southward genome is not expressed and is instead integrated into the bacteria's genome to form the prophage.^[7] In its inactive form, a prophage gets passed on each time the host cell divides. If prophages become active, they can get out the bacterial chromosome and enter the lytic cycle, where they undergo DNA copying, protein synthesis, phage assembly, and lysis.^[8] Since the bacteriophage's genetic information is incorporated into the bacteria's genetic information every bit a prophage, the bacteriophage replicates passively as the bacterium divides to grade daughter bacteria cells.^[7] In this scenario, the daughter bacteria cells incorporate prophage and are known as lysogens. Lysogens can remain in the lysogenic cycle for many generations simply can switch to the lytic cycle at whatever time via a process known equally induction.^[vii] During consecration, prophage DNA is excised from the bacterial genome and is transcribed and translated to make coat proteins for the virus and regulate lytic growth.^[7]

An example of a virus that uses the lysogenic cycle to its advantage is the Herpes Simplex Virus.^[10] Later on showtime entering the lytic cycle and infecting a human host, it enters the lysogenic cycle. This allows it to travel to the nervous system's sensory neurons and remain undetected for long periods of time. In the instance of genital canker, latency is established in lumbosacral dorsal root ganglia, spinal nerve neurons.^[11] The herpes virus can then exit this fallow stage and re-enter the lytic cycle, causing disease symptoms. Thus, while herpes viruses can enter both the lytic and lysogenic cycles, latency allows the virus to survive and evade detection past the immune arrangement due to low viral factor expression.

The model organism for studying lysogeny is the lambda phage. Prophage integration (also known as homologous recombination), maintenance of lysogeny, induction, and command of phage genome excision in induction is described in detail in the lambda phage article.^[12]

Fitness tradeoffs for bacteria [edit]

Bacteriophages are parasitic because they infect their hosts, use bacterial machinery to replicate, and ultimately lyse the bacteria. Temperate phages tin lead to both advantages and disadvantages for their hosts via the lysogenic cycle. During the lysogenic cycle, the virus genome is incorporated as prophage and a repressor prevents viral replication. Nonetheless, a temperate phage can escape repression to replicate, produce viral particles, and lyse the bacteria.^[13] The temperate phage escaping repression would be a disadvantage for the bacteria. On the other mitt, the prophage may transfer genes that enhance host virulence and resistance to the allowed system. Also, the repressor produced past the prophage that prevents prophage genes from being expressed confers immunity for the host bacteria from lytic infection by related viruses.^[13]

Another system, arbitrium, has recently been described for bacteriophages infecting several Bacillus species, in which the decision between lysis and lysogeny is transmitted between bacteria past a peptide factor. ^[xiv] ^[xv]

Lysogenic conversion [edit]

In some interactions between lysogenic phages and leaner, the lysogenic conversion may occur, which can also be called phage conversion. It is when a temperate phage induces a change in the phenotype of the infected bacteria that is not role of a usual phage cycle. Changes can often involve the external membrane of the cell by making it impervious to other phages or even by increasing the pathogenic capability of the bacteria for a host. In this style, temperate bacteriophages besides play a office in the spread of virulence factors, such every bit exotoxins and exoenzymes, among leaner. This alter and so stays in the genome of the infected leaner and is copied and passed down to daughter cells.

Bacterial survival [edit]

Lysogenic conversion has shown to enable biofilm formation in Bacillus anthracis ^[16] Strains of B. anthracis cured of all phage were unable to class biofilms, which are surface-adhered bacterial communities that enable leaner to better admission nutrients and survive environmental stresses.^[17] In addition to biofilm formation in B. anthracis, lysogenic conversion of Bacillus subtilis, Bacillus thuringiensis, and Bacillus cereus has shown an enhanced rate or extent of sporulation.^[16] Sporulation produces endospores, which are metabolically dormant forms of the bacteria that are highly resistant to temperature, ionizing radiations, desiccation, antibiotics, and disinfectants.^[16]

Bacterial virulence [edit]

Non-virulent bacteria accept also been shown to transform into highly virulent pathogens through lysogenic conversion with the virulence factors carried on the lysogenic prophage.^[eighteen] Virulence genes carried within prophages as detached autonomous genetic elements, known as morons, confer an advantage to the leaner that indirectly benefits the virus through enhanced lysogen survival.^[xvi]

Examples:

Corynebacterium diphtheriae produces the toxin of diphtheria only when it is infected past the phage β. In this case, the gene that codes for the toxin is carried past the phage, non the bacterium.^[nineteen]
Vibrio cholerae is a non-toxic strain that can become toxic, producing cholera toxin, when information technology is infected with the phage CTXφ.
Shigella dysenteriae, which produces dysentery has toxins that fall into two major groups, Stx1 and Stx2, whose genes are considered to exist function of the genome of lambdoid prophages.
Streptococcus pyogenes, produce a pyrogenic exotoxin, obtained by lysogenic conversion, which causes fever and a scarlet-cerise rash, carmine fever.
Sure strains of Clostridium botulinum, which causes botulism, express botulinum toxin from phage-tranduced genes.

Preventing lysogenic induction [edit]

Strategies to combat certain bacterial infections by blocking prophage consecration (the transition from the lytic cycle to the lysogenic cycle) by eliminating in vivo induction agents have been proposed.^[18] Reactive oxygen species (ROS), such as hydrogen peroxide, are strong oxidizing agents that can decompose into free radicals and crusade Dna damage to bacteria, which lead to prophage induction.^[18] One potential strategy to gainsay prophage induction is through the utilize of glutathione, a stiff antioxidant that can remove gratis radical intermediates.^[xviii] Another arroyo could be to cause overexpression of CI repressor since prophage induction only occurs when the concentration of CI repressor is likewise low.^[18]

References [edit]

^ ^a ^b ^c Campbell and Reece (2005). Biological science. San Francisco: Pearson. pp. 338–339.
^ Lodish; et al. (2008). Molecular Jail cell Biology. New York: Due west.H. Freeman. pp. 158–159.
^ "Bacteriophages (article) | Viruses". Khan Academy . Retrieved 2022-03-15 .
^ Quiberoni, A.; Suárez, Five. B.; Binetti, A. G.; Reinheimer, J. A. (2011-01-01), "BACTERIOPHAGE | Biological Aspects", in Fuquay, John Due west. (ed.), Encyclopedia of Dairy Sciences (Second Edition), San Diego: Academic Press, pp. 430–438, ISBN978-0-12-374407-four , retrieved 2022-03-15
^ "three.0". seaphagesphagediscoveryguide.helpdocsonline.com . Retrieved 2022-03-15 .
^ Quiberoni, A.; Suárez, 5. B.; Binetti, A. G.; Reinheimer, J. A. (2011-01-01), "BACTERIOPHAGE | Biological Aspects", in Fuquay, John W. (ed.), Encyclopedia of Dairy Sciences (2d Edition), San Diego: Bookish Press, pp. 430–438, ISBN978-0-12-374407-4 , retrieved 2022-03-xv
^ ^a ^b ^c ^d Watson; et al. (2008). Molecular Biology of the Cistron. Cold Leap Harbor, New York: Cold Bound Harbor Laboratory Press. pp. 784–786.
^ "Bacteriophages (article) | Viruses". Khan Academy . Retrieved 2022-03-15 .
^ "Viral replication". THINKER Problems . Retrieved 2021-09-11 .
^ Brown, Jay C. (2017). "Herpes Simplex Virus Latency: The Dna Repair-Centered Pathway". Advances in Virology. 2017: 7028194. doi:10.1155/2017/7028194. ISSN 1687-8639. PMC5309397. PMID 28255301.
^ Awasthi, Sita; Friedman, Harvey M. (2014-03-xv). "A Paradigm Shift: Vaccine-Induced Antibodies equally an Allowed Correlate of Protection Against Herpes Simplex Virus Type 1 Genital Herpes". The Periodical of Infectious Diseases. 209 (half dozen): 813–815. doi:ten.1093/infdis/jit658. ISSN 0022-1899. PMID 24285847.
^ "3.0". seaphagesphagediscoveryguide.helpdocsonline.com . Retrieved 2022-03-15 .
^ ^a ^b Chen; et al. (21 June 2005). "Population Fitness and the Regulation of Escherichia coli Genes by Bacterial Viruses". PLOS Biology. iii (7): e229. doi:10.1371/periodical.pbio.0030229. PMC1151598. PMID 15984911.
^ Callaway, Ewen (2017). "Do you speak virus? Phages caught sending chemical messages". Nature. doi:10.1038/nature.2017.21313. Archived from the original on 2019-09-29. Retrieved 2019-09-11 .
^ Stokar-Avihail A, Tal N, Erez Z, Lopatina A, Sorek R. Widespread Utilization of Peptide Communication in Phages Infecting Soil and Pathogenic Bacteria. Cell host & microbe. 2019 May 8;25(5):746-55.
^ ^a ^b ^c ^d Louis-Charles Fortier; et al. (23 Apr 2013). "Importance of prophages to development and virulence of bacterial pathogens". Virulence. 4 (v): 354–65. doi:10.4161/viru.24498. PMC3714127. PMID 23611873.
^ Nadell; et al. (thirteen July 2011). "A fitness merchandise-off between local competition and dispersal in Vibrio cholerae biofilms". PNAS. 108 (34): 14181–14185. Bibcode:2011PNAS..10814181N. doi:10.1073/pnas.1111147108. PMC3161532. PMID 21825170.
^ ^a ^b ^c ^d ^{due east} Smashing, Eric C. (14 Dec 2012). "Paradigms of pathogenesis: targeting the mobile genetic elements of disease". Frontiers in Cellular and Infection Microbiology. ii: 161. doi:ten.3389/fcimb.2012.00161. PMC3522046. PMID 23248780.
^ Mokrousov I (January 2009). "Corynebacterium diphtheriae: genome diversity, population construction and genotyping perspectives". Infection, Genetics and Development. 9 (one): i–xv. doi:ten.1016/j.meegid.2008.09.011. PMID 19007916.