Lysogenic cycle

Last updated
Lysogenic cycle, compared to lytic cycle Phage2.JPG
Lysogenic cycle, compared to lytic cycle
Lysogenic Cycle:1. The prokaryotic cell is shown with its DNA, in green. 2. The bacteriophage attaches and releases its DNA, shown in red, into the prokaryotic cell. 3. The phage DNA then moves through the cell to the host's DNA. 4. The phage DNA integrates itself into the host cell's DNA, creating prophage. 5. The prophage then remains dormant until the host cell divides. 6. After the host cell has divided, the phage DNA in the daughter cells activate, and the phage DNA begins to express itself. Some of the cells containing the prophage go on to create new phages which will move on to infect other cells. Lysogentic cycle diagram.svg
Lysogenic Cycle:1. The prokaryotic cell is shown with its DNA, in green. 2. The bacteriophage attaches and releases its DNA, shown in red, into the prokaryotic cell. 3. The phage DNA then moves through the cell to the host's DNA. 4. The phage DNA integrates itself into the host cell's DNA, creating prophage. 5. The prophage then remains dormant until the host cell divides. 6. After the host cell has divided, the phage DNA in the daughter cells activate, and the phage DNA begins to express itself. Some of the cells containing the prophage go on to create new phages which will move on to infect other cells.

Lysogeny, or the lysogenic cycle, is one of two cycles of viral reproduction (the lytic cycle 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 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]

Contents

Lysogenic cycles can also occur in eukaryotes, although the method of DNA incorporation is not fully understood. For instance, the AIDS viruses can either infect humans (or some other primates) lytically, or lay dormant (lysogenic) as part of the infected cells' genome, keeping the ability to return to lysis at a later time. The rest of this article is about lysogeny in bacterial hosts.

The difference between lysogenic and lytic cycles is that, in lysogenic cycles, the spread of the viral DNA occurs through the usual prokaryotic reproduction, whereas a lytic cycle is more immediate in that it results in many copies of the virus being created very quickly and the cell is destroyed. One key difference between the lytic cycle and the lysogenic cycle is that the latter does not lyse the host cell straight away. [2] Phages that replicate only via the lytic cycle are known as virulent phages while phages that replicate using both lytic and lysogenic cycles are known as temperate phages. [1]

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 exit the bacterial chromosome to initiate the lytic cycle. [1] In the lysogenic cycle the host DNA is not hydrolyzed but in the lytic cycle the host DNA is hydrolyzed in the lytic phase.

Bacteriophages

Bacteriophages are viruses that infect and replicate within 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 cycle to enter depends on a variety of factors. [3] For instance, if there are several other infecting phages (or if there is a high multiplicity), it is likely that the phage will use the lysogenic cycle. This may be 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 cycle if it is exposed to DNA-damaging agents, such as UV radiation and chemicals. Other factors with the potential to induce temperate phage release include temperature, pH, osmotic pressure, and low nutrient concentration. [4] However, phages may also re-enter the lytic cycle spontaneously. In 80-90% of single-cell infections, phages enter the lysogenic cycle. In the other 10-20%, phages enter the lytic cycle.[ citation needed ]

Evidence of Lysogeny

It is sometimes possible to detect which cycle a phage enters by looking at the plaque morphology in bacterial plate culture. [5] Since phages that enter the lytic cycle kill the host bacterial cells, plaques will appear clear (photo A). The plaques may also appear to have a halo-like ring around the edge, indicating that these cells were not fully lysed. In contrast, infecting phages that enter the lysogenic cycle will 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 rule are also known to exist, where non-temperate phages still exhibit cloudy plaques, and temperate phage mutants can generate clear plaques as a result of loss of lysogen formation ability.[ citation needed ]

See a comparison 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, DNA extraction, or propagation on sensitive strains. [4]

Via the lysogenic cycle, the bacteriophage's genome is not expressed and is instead integrated into the bacteria's genome to form the prophage. [6] In its inactive form, a prophage gets passed on each time the host cell divides. If prophages become active, they can exit the bacterial chromosome and enter the lytic cycle, where they undergo DNA copying, protein synthesis, phage assembly, and lysis. [3] Since the bacteriophage's genetic information is incorporated into the bacteria's genetic information as a prophage, the bacteriophage replicates passively as the bacterium divides to form daughter bacteria cells. [6] In this scenario, the daughter bacteria cells contain prophage and are known as lysogens. Lysogens can remain in the lysogenic cycle for many generations but can switch to the lytic cycle at any time via a process known as induction. [6] During induction, prophage DNA is excised from the bacterial genome and is transcribed and translated to make coat proteins for the virus and regulate lytic growth. [6]

Lysogenic Cycle Viral Replication.png
Lysogenic Cycle

An example of a virus that uses the lysogenic cycle to its advantage is the Herpes Simplex Virus. [8] After first 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 case of genital herpes, latency is established in lumbosacral dorsal root ganglia, spinal nerve neurons. [9] The herpes virus can then exit this dormant 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 by the immune system due to low viral gene expression.

The model organism for studying lysogeny is the lambda phage. Prophage integration (also known as homologous recombination), maintenance of lysogeny, induction, and control of phage genome excision in induction is described in detail in the lambda phage article. [5]

Fitness tradeoffs for bacteria

Bacteriophages are parasitic because they infect their hosts, use bacterial machinery to replicate, and ultimately lyse the bacteria. Temperate phages can 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. [10] The temperate phage escaping repression would be a disadvantage for the bacteria. On the other hand, the prophage may transfer genes that enhance host virulence and resistance to the immune system. Also, the repressor produced by the prophage that prevents prophage genes from being expressed confers immunity for the host bacteria from lytic infection by related viruses. [10]

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 by a peptide factor. [11] [12]

Lysogenic conversion

In some interactions between lysogenic phages and bacteria, 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 part 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 way, temperate bacteriophages also play a role in the spread of virulence factors, such as exotoxins and exoenzymes, amongst bacteria. This change then stays in the genome of the infected bacteria and is copied and passed down to daughter cells.

Bacterial survival

Lysogenic conversion has shown to enable biofilm formation in Bacillus anthracis [13] Strains of B. anthracis cured of all phage were unable to form biofilms, which are surface-adhered bacterial communities that enable bacteria to better access nutrients and survive environmental stresses. [14] 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. [13] Sporulation produces endospores, which are metabolically dormant forms of the bacteria that are highly resistant to temperature, ionizing radiation, desiccation, antibiotics, and disinfectants. [13]

Bacterial virulence

Non-virulent bacteria have also been shown to transform into highly virulent pathogens through lysogenic conversion with the virulence factors carried on the lysogenic prophage. [15] Virulence genes carried within prophages as discrete autonomous genetic elements, known as morons, confer an advantage to the bacteria that indirectly benefits the virus through enhanced lysogen survival. [13]

Examples:

Preventing lysogenic induction

Strategies to combat certain bacterial infections by blocking prophage induction (the transition from the lytic cycle to the lysogenic cycle) by eliminating in vivo induction agents have been proposed. [15] Reactive oxygen species (ROS), such as hydrogen peroxide, are strong oxidizing agents that can decompose into free radicals and cause DNA damage to bacteria, which lead to prophage induction. [15] One potential strategy to combat prophage induction is through the use of glutathione, a strong antioxidant that can remove free radical intermediates. [15] Another approach could be to cause overexpression of CI repressor since prophage induction only occurs when the concentration of CI repressor is too low. [15]

Related Research Articles

<span class="mw-page-title-main">Bacteriophage</span> Virus that infects and replicates within bacteria

A bacteriophage, also known informally as a phage, is a virus that infects and replicates within bacteria and archaea. The term was derived from "bacteria" and the Greek φαγεῖν, meaning "to devour". Bacteriophages are composed of proteins that encapsulate a DNA or RNA genome, and may have structures that are either simple or elaborate. Their genomes may encode as few as four genes and as many as hundreds of genes. Phages replicate within the bacterium following the injection of their genome into its cytoplasm.

<span class="mw-page-title-main">Lambda phage</span> Bacteriophage that infects Escherichia coli

Enterobacteria phage λ is a bacterial virus, or bacteriophage, that infects the bacterial species Escherichia coli. It was discovered by Esther Lederberg in 1950. The wild type of this virus has a temperate life cycle that allows it to either reside within the genome of its host through lysogeny or enter into a lytic phase, during which it kills and lyses the cell to produce offspring. Lambda strains, mutated at specific sites, are unable to lysogenize cells; instead, they grow and enter the lytic cycle after superinfecting an already lysogenized cell.

A provirus is a virus genome that is integrated into the DNA of a host cell. In the case of bacterial viruses (bacteriophages), proviruses are often referred to as prophages. However, proviruses are distinctly different from prophages and these terms should not be used interchangeably. Unlike prophages, proviruses do not excise themselves from the host genome when the host cell is stressed.

A lysogen or lysogenic bacterium is a bacterial cell which can produce and transfer the ability to produce a phage. A prophage is either integrated into the host bacteria's chromosome or more rarely exists as a stable plasmid within the host cell. The prophage expresses gene(s) that repress the phage's lytic action, until this repression is disrupted. Currently a variety of studies are being conducted to see whether other genes are active during lysogeny, examples of which include phage-encoded tRNA and virulence genes.

<span class="mw-page-title-main">Prophage</span> Bacteriophage genome that is integrated into a bacterial cell

A prophage is a bacteriophage genome that is integrated into the circular bacterial chromosome or exists as an extrachromosomal plasmid within the bacterial cell. Integration of prophages into the bacterial host is the characteristic step of the lysogenic cycle of temperate phages. Prophages remain latent in the genome through multiple cell divisions until activation by an external factor, such as UV light, leading to production of new phage particles that will lyse the cell and spread. As ubiquitous mobile genetic elements, prophages play important roles in bacterial genetics and evolution, such as in the acquisition of virulence factors.

Virulence is a pathogen's or microorganism's ability to cause damage to a host.

<span class="mw-page-title-main">Transduction (genetics)</span> Transfer process in genetics

Transduction is the process by which foreign DNA is introduced into a cell by a virus or viral vector. An example is the viral transfer of DNA from one bacterium to another and hence an example of horizontal gene transfer. Transduction does not require physical contact between the cell donating the DNA and the cell receiving the DNA, and it is DNase resistant. Transduction is a common tool used by molecular biologists to stably introduce a foreign gene into a host cell's genome.

<span class="mw-page-title-main">Lytic cycle</span> Cycle of viral reproduction

The lytic cycle is one of the two cycles of viral reproduction, the other being the lysogenic cycle. The lytic cycle results in the destruction of the infected cell and its membrane. Bacteriophages that only use the lytic cycle are called virulent phages.

In virology, temperate refers to the ability of some bacteriophages to display a lysogenic life cycle. Many temperate phages can integrate their genomes into their host bacterium's chromosome, together becoming a lysogen as the phage genome becomes a prophage. A temperate phage is also able to undergo a productive, typically lytic life cycle, where the prophage is expressed, replicates the phage genome, and produces phage progeny, which then leave the bacterium. With phage the term virulent is often used as an antonym to temperate, but more strictly a virulent phage is one that has lost its ability to display lysogeny through mutation rather than a phage lineage with no genetic potential to ever display lysogeny.

Salmonella virus P22 is a bacteriophage in the Podoviridae family that infects Salmonella typhimurium. Like many phages, it has been used in molecular biology to induce mutations in cultured bacteria and to introduce foreign genetic material. P22 has been used in generalized transduction and is an important tool for investigating Salmonella genetics.

P1 is a temperate bacteriophage that infects Escherichia coli and some other bacteria. When undergoing a lysogenic cycle the phage genome exists as a plasmid in the bacterium unlike other phages that integrate into the host DNA. P1 has an icosahedral head containing the DNA attached to a contractile tail with six tail fibers. The P1 phage has gained research interest because it can be used to transfer DNA from one bacterial cell to another in a process known as transduction. As it replicates during its lytic cycle it captures fragments of the host chromosome. If the resulting viral particles are used to infect a different host the captured DNA fragments can be integrated into the new host's genome. This method of in vivo genetic engineering was widely used for many years and is still used today, though to a lesser extent. P1 can also be used to create the P1-derived artificial chromosome cloning vector which can carry relatively large fragments of DNA. P1 encodes a site-specific recombinase, Cre, that is widely used to carry out cell-specific or time-specific DNA recombination by flanking the target DNA with loxP sites.

<span class="mw-page-title-main">Mobilome</span>

The mobilome is the entire set of mobile genetic elements in a genome. Mobilomes are found in eukaryotes, prokaryotes, and viruses. The compositions of mobilomes differ among lineages of life, with transposable elements being the major mobile elements in eukaryotes, and plasmids and prophages being the major types in prokaryotes. Virophages contribute to the viral mobilome.

<i>Corticovirus</i> Genus of viruses

Corticovirus is a genus of viruses in the family Corticoviridae. Corticoviruses are bacteriophages; that is, their natural hosts are bacteria. The genus contains two species. The name is derived from Latin cortex, corticis. However, prophages closely related to PM2 are abundant in the genomes of aquatic bacteria, suggesting that the ecological importance of corticoviruses might be underestimated. Bacteriophage PM2 was first described in 1968 after isolation from seawater sampled from the coast of Chile.

<span class="mw-page-title-main">Phage typing</span>

Phage typing is a phenotypic method that uses bacteriophages for detecting and identifying single strains of bacteria. Phages are viruses that infect bacteria and may lead to bacterial cell lysis. The bacterial strain is assigned a type based on its lysis pattern. Phage typing was used to trace the source of infectious outbreaks throughout the 1900s, but it has been replaced by genotypic methods such as whole genome sequencing for epidemiological characterization.

<span class="mw-page-title-main">Bacteriophage P2</span> Species of virus

Bacteriophage P2, scientific name Escherichia virus P2, is a temperate phage that infects E. coli. It is a tailed virus with a contractile sheath and is thus classified in the genus Peduovirus, subfamily Peduovirinae, family Myoviridae within order Caudovirales. This genus of viruses includes many P2-like phages as well as the satellite phage P4.

The CTXφ bacteriophage is a filamentous bacteriophage. It is a positive-strand DNA virus with single-stranded DNA (ssDNA).

Bacteriophage T12 is a bacteriophage that infects Streptococcus pyogenes bacteria. It is a proposed species of the family Siphoviridae in the order Caudovirales also known as tailed viruses. It converts a harmless strain of bacteria into a virulent strain. It carries the speA gene which codes for erythrogenic toxin A. speA is also known as streptococcal pyogenic exotoxin A, scarlet fever toxin A, or even scarlatinal toxin. Note that the name of the gene "speA" is italicized; the name of the toxin "speA" is not italicized. Erythrogenic toxin A converts a harmless, non-virulent strain of Streptococcus pyogenes to a virulent strain through lysogeny, a life cycle which is characterized by the ability of the genome to become a part of the host cell and be stably maintained there for generations. Phages with a lysogenic life cycle are also called temperate phages. Bacteriophage T12, proposed member of family Siphoviridae including related speA-carrying bacteriophages, is also a prototypic phage for all the speA-carrying phages of Streptococcus pyogenes, meaning that its genome is the prototype for the genomes of all such phages of S. pyogenes. It is the main suspect as the cause of scarlet fever, an infectious disease that affects small children.

Mycobacterium virus D29 (D29) is a cluster A mycobacteriophage belonging to the Siphoviridae family of viruses, it was discovered in 1954 by S. Froman. D29 is notable for its ability to infect M. tuberculosis. D29 is a double stranded DNA mycobacteriophage. It is a lytic phage, this means that D29 takes the lytic pathway of infection instead of the lysogenic pathway of infection. There are no human associated diseases associated with mycobacterium virus D29.

Escherichia virus CC31, formerly known as Enterobacter virus CC31, is a dsDNA bacteriophage of the subfamily Tevenvirinae responsible for infecting the bacteria family of Enterobacteriaceae. It is one of two discovered viruses of the genus Karamvirus, diverging away from the previously discovered T4virus, as a clonal complex (CC). CC31 was first isolated from Escherichia coli B strain S/6/4 and is primarily associated with Escherichia, even though is named after Enterobacter.

Arbitrium is a viral peptide produced by bacteriophages to communicate with each other and decide host cell fate. It is six amino acids(aa) long, and so is also referred to as a hexapeptide. It is produced when a phage infects a bacterial host. and signals to other phages that the host has been infected.

References

  1. 1 2 3 Campbell and Reece (2005). Biology. San Francisco: Pearson. pp. 338–339.
  2. ↑ Lodish; et al. (2008). Molecular Cell Biology. New York: W.H. Freeman. pp. 158–159.
  3. 1 2 "Bacteriophages (article) | Viruses". Khan Academy. Retrieved 2022-03-15.
  4. 1 2 Quiberoni, A.; Suárez, V. B.; Binetti, A. G.; Reinheimer, J. A. (2011-01-01), "BACTERIOPHAGE | Biological Aspects", in Fuquay, John W. (ed.), Encyclopedia of Dairy Sciences (Second Edition), San Diego: Academic Press, pp. 430–438, ISBN   978-0-12-374407-4 , retrieved 2022-03-15
  5. 1 2 "3.0". seaphagesphagediscoveryguide.helpdocsonline.com. Retrieved 2022-03-15.
  6. 1 2 3 4 Watson; et al. (2008). Molecular Biology of the Gene. Cold Spring Harbor, New York: Cold Spring Harbor Laboratory Press. pp. 784–786.
  7. ↑ "Viral replication". THINKER BUG. Retrieved 2021-09-11.
  8. ↑ 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. PMC   5309397 . PMID   28255301.
  9. ↑ Awasthi, Sita; Friedman, Harvey M. (2014-03-15). "A Paradigm Shift: Vaccine-Induced Antibodies as an Immune Correlate of Protection Against Herpes Simplex Virus Type 1 Genital Herpes". The Journal of Infectious Diseases. 209 (6): 813–815. doi:10.1093/infdis/jit658. ISSN   0022-1899. PMID   24285847.
  10. 1 2 Chen; et al. (21 June 2005). "Population Fitness and the Regulation of Escherichia coli Genes by Bacterial Viruses". PLOS Biology. 3 (7): e229. doi: 10.1371/journal.pbio.0030229 . PMC   1151598 . PMID   15984911. Open Access logo PLoS transparent.svg
  11. ↑ 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.
  12. ↑ 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.
  13. 1 2 3 4 Louis-Charles Fortier; et al. (23 April 2013). "Importance of prophages to evolution and virulence of bacterial pathogens". Virulence. 4 (5): 354–65. doi:10.4161/viru.24498. PMC   3714127 . PMID   23611873.
  14. ↑ Nadell; et al. (13 July 2011). "A fitness trade-off between local competition and dispersal in Vibrio cholerae biofilms". PNAS. 108 (34): 14181–14185. Bibcode:2011PNAS..10814181N. doi: 10.1073/pnas.1111147108 . PMC   3161532 . PMID   21825170.
  15. 1 2 3 4 5 Keen, Eric C. (14 December 2012). "Paradigms of pathogenesis: targeting the mobile genetic elements of disease". Frontiers in Cellular and Infection Microbiology. 2: 161. doi: 10.3389/fcimb.2012.00161 . PMC   3522046 . PMID   23248780.
  16. ↑ Mokrousov I (January 2009). "Corynebacterium diphtheriae: genome diversity, population structure and genotyping perspectives". Infection, Genetics and Evolution. 9 (1): 1–15. doi:10.1016/j.meegid.2008.09.011. PMID   19007916.
This page is based on this Wikipedia article
Text is available under the CC BY-SA 4.0 license; additional terms may apply.
Images, videos and audio are available under their respective licenses.