Viral tropism is determined by a combination of susceptibility and permissiveness: a host cell must be both permissive allow viral entry and susceptible possess the receptor complement needed for viral entry for a virus to establish infection.
T helper cells, macrophages or dendritic cells. These cells express a CD4 receptor, to which the HIV virus can bind, through the gp and gp41 proteins on its surface. In virology, Tissue tropism is the cells and tissues of a host that support growth of a particular virus or bacteria. Some viruses have a broad tissue tropism and can infect many types of cells and tissues. Other viruses may infect primarily a single tissue.
Factors influencing viral tissue tropism include: 1 the presence of cellular receptors permitting viral entry, 2 availability of transcription factors involved in viral replication, 3 the molecular nature of the viral tropogen, and 4 the cellular receptors are the proteins found on a cell or viral surface. These receptors are like keys allowing the viral cell to fuse with a cell or attach itself to a cell.
The way that these proteins are acquired is through similar process to that of an infection cycle. Therefore, HIV can enter T cells and macrophages. 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 are viruses that affect plants. Like all other viruses, plant viruses are obligate intracellular parasites that do not have the molecular machinery to replicate without a host.
Plant viruses are pathogenic to higher plants. There are many types of plant virus, but often they only cause a loss of yield, and it is not economically viable to try to control them. Plant viruses are often spread from plant to plant by organisms vectors. These are normally insects, but some fungi, nematode worms and single-celled organisms have been shown to be vectors. When control of plant virus infections is considered economical, for perennial fruits for example , efforts are concentrated on killing the vectors and removing alternate hosts such as weeds.
Plant viruses are harmless to humans and other animals because they can only reproduce in living plant cells. To enter the cells, proteins on the surface of the virus interact with proteins of the cell. Attachment, or adsorption, occurs between the viral particle and the host cell membrane. A hole forms in the cell membrane, then the virus particle or its genetic contents are released into the host cell, where viral reproduction may commence.
At this stage, a distinction between susceptibility and permissibility of a host cell is made. Permissibility determines the outcome of the infection. After control is established and the environment is set for the virus to begin making copies of itself, replication occurs quickly by the millions. After a virus has made many copies of itself, it usually has exhausted the cell of its resources. The host cell is now no longer useful to the virus, therefore the cell often dies and the newly produced viruses must find a new host.
The process by which virus progeny are released to find new hosts, is called shedding. This is the final stage in the viral life cycle. This hiding is deemed latency.
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