How Do Enveloped Animal Viruses Exit Their Host?
21.2C: Beast Viruses
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- 13548
Beast viruses have their genetic material copied by a host cell after which they are released into the surround to cause disease.
Learning Objectives
- Depict various animal viruses and the diseases they cause
Cardinal Points
- Animal viruses may enter a host cell by either receptor -mediated endocytosis or by changing shape and inbound the jail cell through the cell membrane.
- Viruses crusade diseases in humans and other animals; they often have to run their form before symptoms disappear.
- Examples of viral animal diseases include hepatitis C, chicken pox, and shingles.
Key Terms
- receptor-mediated endocytosis: a process by which cells internalize molecules (endocytosis) by the inward budding of plasma membrane vesicles containing proteins with receptor sites specific to the molecules being internalized
Creature Viruses
Fauna viruses, unlike the viruses of plants and bacteria, do non have to penetrate a cell wall to gain access to the host cell. Not-enveloped or "naked" creature viruses may enter cells in ii different ways. When a poly peptide in the viral capsid binds to its receptor on the host jail cell, the virus may be taken inside the cell via a vesicle during the normal prison cell procedure 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. The viral genome is then "injected" into the host cell through these channels in a manner analogous to that used by many bacteriophages. Enveloped viruses also have two ways of inbound cells afterwards binding to their receptors: receptor-mediated endocytosis and fusion. Many enveloped viruses enter the cell past receptor-mediated endocytosis in a fashion like to some not-enveloped viruses. On the other mitt, fusion only occurs with enveloped virions. These viruses, which include HIV amidst others, use special fusion proteins in their envelopes to crusade the envelope to fuse with the plasma membrane of the cell, thus releasing the genome and capsid of the virus into the jail cell cytoplasm.
Subsequently making their proteins and copying their genomes, animal viruses complete the assembly of new virions and leave the cell. Using the example of HIV, enveloped brute viruses may bud from the jail cell membrane equally they assemble themselves, taking a piece of the cell'southward plasma membrane in the process. On the other mitt, non-enveloped viral progeny, such as rhinoviruses, accumulate in infected cells until in that location is a bespeak for lysis or apoptosis, and all virions are released together.
Fauna 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 emptying of the virus from the body by the allowed system with eventual recovery from the infection. Examples of astute viral diseases are the common common cold and influenza. Other viruses cause long-term chronic infections, such as the virus causing hepatitis C, whereas others, similar herpes simplex virus, cause only intermittent symptoms. Notwithstanding other viruses, such as human being herpes viruses half-dozen and 7, which in some cases can cause the minor babyhood 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 but detected by routine blood work on patients with gamble factors such as intravenous drug utilize. Since many of the symptoms of viral diseases are caused by immune responses, a lack of symptoms is an indication of a weak allowed response to the virus. This allows the virus to escape elimination by the immune arrangement and persist in individuals for years, while continuing to produce depression levels of progeny virions in what is known equally 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 later on the initial infection.
As mentioned, canker simplex virus can remain in a state of latency in nervous tissue for months, even years. As the virus "hides" in the tissue and makes few if whatever viral proteins, there is nothing for the immune response to act confronting; immunity to the virus slowly declines. Nether certain weather condition, including various types of physical and psychological stress, the latent canker simplex virus may be reactivated and undergo a lytic replication cycle in the peel, causing the lesions associated with the disease. Once virions are produced in the peel 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 likewise, including the varicella-zoster virus that causes chickenpox. After having a chickenpox infection in childhood, the varicella-zoster virus tin remain latent for many years and reactivate in adults to cause the painful status known as "shingles".
Source: https://bio.libretexts.org/Bookshelves/Introductory_and_General_Biology/Book%3A_General_Biology_(Boundless)/21%3A_Viruses/21.2%3A_Virus_Infections_and_Hosts/21.2C%3A_Animal_Viruses
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