What is the difference between lysogeny and latency

The virus remains dormant until host conditions deteriorate, perhaps due to depletion of nutrients; then, the endogenous phages known as prophages become active. At this point they initiate the reproductive cycle, resulting in lysis of the host cell. An example of a bacteriophage known to follow the lysogenic cycle and the lytic cycle is the phage lambda of E. Viruses that infect plant or animal cells may also undergo infections where they are not producing virions for long periods. An example is the animal herpes viruses, including herpes simplex viruses, which cause oral and genital herpes in humans.

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. When plant viruses are transferred between different plants, this is known as horizontal transmission; when they are inherited from a parent, this is called vertical transmission. Symptoms of viral diseases vary according to the virus and its host.

One common symptom is hyperplasia: the abnormal proliferation of cells that causes the appearance of plant tumors known as galls. Other viruses induce hypoplasia, or decreased cell growth, in the leaves of plants, causing thin, yellow areas to appear. Still other viruses affect the plant by directly killing plant cells; a process known as cell necrosis. Other symptoms of plant viruses include malformed leaves, black streaks on the stems of the plants, altered growth of stems, leaves, or fruits, and ring spots, which are circular or linear areas of discoloration found in a leaf.

Oak tree galls : Galls are abnormal plant growth or swellings comprised of plant tissue. Even the smallest and simplest of cells, prokaryotic bacteria, may be attacked by specific types of viruses.

Bacteriophages are viruses that infect bacteria. Bacteriophages may have a lytic cycle or a lysogenic cycle, and a few viruses are capable of carrying out both.

When infection of a cell by a bacteriophage results in the production of new virions, the infection is said to be productive. With lytic phages, bacterial cells are broken open lysed and destroyed after immediate replication of the virion.

As soon as the cell is destroyed, the phage progeny can find new hosts to infect. An example of a lytic bacteriophage is T4, which infects E. Lytic phages are more suitable for phage therapy. Some lytic phages undergo a phenomenon known as lysis inhibition, where completed phage progeny will not immediately lyse out of the cell if extracellular phage concentrations are high.

In contrast, the lysogenic cycle does not result in immediate lysing of the host cell. Those phages able to undergo lysogeny are known as temperate phages. Viral protein expressed primarily to establish, maintain or terminate latency, the part of the viral life cycle during which a virus lies dormant latent within a cell. This part of the virus life cycle is called the lysogenic part in prokaryotic viruses. During latency, the viral genome can either exist as a provirus integrated in the host genome proviral latency or as a linear or circular plasmid in the host cell episomal latency.

The virus does not replicate, but is passively duplicated when the host divides.