Learning Objectives Describe the lytic and lysogenic cycles of bacteriophages. Key Points Viruses are species specific, but almost every species on Earth can be affected by some form of virus. The lytic cycle involves the reproduction of viruses using a host cell to manufacture more viruses; the viruses then burst out of the cell.
The lysogenic cycle involves the incorporation of the viral genome into the host cell genome, infecting it from within. Key Terms latency : The ability of a pathogenic virus to lie dormant within a cell.
Different Hosts and Their Viruses Viruses are often very specific as to which hosts and which cells within the host they will infect. Bacteriophages Bacteriophages are viruses that infect bacteria. In the lytic cycle, the phage replicates and lyses the host cell.
Once inside the host cell, some viruses, such as herpes and HIV, do not reproduce right away. Instead, they mix their genetic instructions into the host cell's genetic instructions.
When the host cell reproduces, the viral genetic instructions get copied into the host cell's offspring. The host cells may undergo many rounds of reproduction, and then some environmental or predetermined genetic signal will stir the "sleeping" viral instructions. The viral genetic instructions will then take over the host's machinery and make new viruses as described above. This cycle, called the lysogenic cycle , is shown in the accompanying figure.
The phage then uses the host cell to synthesize the remaining proteins required to build new phage particles. The heads and sheaths are assembled separately, the new genetic material packed into the head and new daughter phage particles constructed. During this process, the host cells gradually become weakened by phage enzymes and eventually burst, releasing on average new phage progeny into the surrounding environment.
Figure 2. Depiction of the stages of the bacteriophage lytic cycle. Watch the lytic cycle in action here. The lysogenic cycle Figure 3 , sometimes referred to as temperate or non-virulent infection, does not kill the host cell, instead using it as a refuge where it exists in a dormant state.
Following the injection of the phage DNA into the host cell, it integrates itself into the host genome, with the help of phage-encoded integrases, where it is then termed a prophage.
The prophage genome is then replicated passively along with the host genome as the host cell divides for as long as it remains there and does not form the proteins required to produce progeny. As the phage genome is generally comparatively small, the bacterial hosts are normally relatively unharmed by this process.
Figure 3. Depiction of the stages of the bacteriophage lysogenic cycle. If a bacterium containing prophage is exposed to stressors, such as UV light, low nutrient conditions, or chemicals like mitomycin C, prophage may spontaneously extract themselves from the host genome and enter the lytic cycle in a process called induction. This process, however, is not perfect and prophage may sometimes leave portions of their DNA behind or take portions of host DNA with them when they re-circularize.
If they then infect a new host cell, they may transport bacterial genes from one strain to another in a process called transduction. This is one method by which antibiotic resistance genes, toxin and superantigen-encoding genes and other virulence traits may spread through a bacterial population.
In a process called latency, these viruses can exist in nervous tissue for long periods of time without producing new virions, only to leave latency periodically and cause lesions in the skin where the virus replicates. Even though there are similarities between lysogeny and latency, the term lysogenic cycle is usually reserved to describe bacteriophages. Animal viruses have their genetic material copied by a host cell after which they are released into the environment to cause disease.
Animal viruses, unlike the viruses of plants and bacteria, do not have to penetrate a cell wall to gain access to the host cell. When a protein in the viral capsid binds to its receptor on the host cell, the virus may be taken inside the cell via a vesicle during the normal cell process of receptor-mediated endocytosis.
An alternative method of cell penetration used by non-enveloped viruses is for capsid proteins to undergo shape changes after binding to the receptor, creating channels in the host cell membrane. Enveloped viruses also have two ways of entering cells after binding to their receptors: receptor-mediated endocytosis and fusion. Many enveloped viruses enter the cell by receptor-mediated endocytosis in a fashion similar to some non-enveloped viruses. On the other hand, fusion only occurs with enveloped virions.
These viruses, which include HIV among others, use special fusion proteins in their envelopes to cause the envelope to fuse with the plasma membrane of the cell, thus releasing the genome and capsid of the virus into the cell cytoplasm. After making their proteins and copying their genomes, animal viruses complete the assembly of new virions and exit the cell. On the other hand, non-enveloped viral progeny, such as rhinoviruses, accumulate in infected cells until there is a signal for lysis or apoptosis, and all virions are released together.
Animal viruses are associated with a variety of human diseases. Some of them follow the classic pattern of acute disease, where symptoms worsen for a short period followed by the elimination of the virus from the body by the immune system with eventual recovery from the infection.
Examples of acute viral diseases are the common cold and influenza. Other viruses cause long-term chronic infections, such as the virus causing hepatitis C, whereas others, like herpes simplex virus, cause only intermittent symptoms.
Still other viruses, such as human herpes viruses 6 and 7, which in some cases can cause the minor childhood disease roseola, often successfully cause productive infections without causing any symptoms at all in the host; these patients have an asymptomatic infection. In hepatitis C infections, the virus grows and reproduces in liver cells, causing low levels of liver damage. The damage is so low that infected individuals are often unaware that they are infected, with many infections only detected by routine blood work on patients with risk factors such as intravenous drug use.
Since many of the symptoms of viral diseases are caused by immune responses, a lack of symptoms is an indication of a weak immune response to the virus. This allows the virus to escape elimination by the immune system and persist in individuals for years, while continuing to produce low levels of progeny virions in what is known as a chronic viral disease.
Chronic infection of the liver by this virus leads to a much greater chance of developing liver cancer, sometimes as much as 30 years after the initial infection. As mentioned, herpes simplex virus can remain in a state of latency in nervous tissue for months, even years. Under certain conditions, including various types of physical and psychological stress, the latent herpes simplex virus may be reactivated and undergo a lytic replication cycle in the skin, causing the lesions associated with the disease.
Once virions are produced in the skin and viral proteins are synthesized, the immune response is again stimulated and resolves the skin lesions in a few days by destroying viruses in the skin. As a result of this type of replicative cycle, appearances of cold sores and genital herpes outbreaks only occur intermittently, even though the viruses remain in the nervous tissue for life.
Latent infections are common with other herpes viruses as well, including the varicella-zoster virus that causes chickenpox. Chicken pox virus : a Varicella-zoster, the virus that causes chickenpox, has an enveloped icosahedral capsid visible in this transmission electron micrograph.
Its double-stranded DNA genome incorporates into the host DNA and reactivates after latency in the form of b shingles, often exhibiting a rash. Plant viruses can cause damage to stems, leaves, and fruits and can have a major impact on the economy because of food supply disruptions. As plant viruses have a cell wall to protect their cells, their viruses do not use receptor-mediated endocytosis to enter host cells as is seen with animal viruses.
This damage is often caused by weather, insects, animals, fire, or human activities such as farming or landscaping. Additionally, plant offspring may inherit viral diseases from parent plants.
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