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. How a phage decides which cycle to enter depends on a variety of factors. 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 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. However, phages may also re-enter the lytic cycle spontaneously.
Evidence of lysogeny It is sometimes possible to detect which cycle a phage enters by looking at the plaque morphology in bacterial plate culture. Generally, clearer plaques indicate more efficient lysis, while cloudy or turbid plaques indicate less efficient lysis. Turbid plaques may indicate that a phage can go through the lysogenic cycle, however there are other reasons that plaques may appear turbid. Detection methods of phages released from the lysogenic cycle include electron microscopy, DNA extraction, or propagation on sensitive strains. 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. An example of a virus that uses the lysogenic cycle to its advantage is the Herpes Simplex Virus. 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. 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.
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. 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.
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. 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. 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. 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. •
Vibrio cholerae is a non-toxic strain that can become toxic, producing
cholera toxin, when it 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 be part of the genome of lambdoid
prophages. •
Streptococcus pyogenes, produce a pyrogenic
exotoxin, obtained by lysogenic conversion, which causes fever and a scarlet-red rash,
scarlet fever. • Certain strains of
Clostridium botulinum, which causes
botulism, express
botulinum toxin from phage-tranduced genes.
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.
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. One potential strategy to combat prophage induction is through the use of
glutathione, a strong
antioxidant that can remove free radical intermediates. Another approach could be to cause overexpression of CI repressor since prophage induction only occurs when the concentration of CI repressor is too low. == References ==