About microscopic forms of life, including Bacteria, Archea, protozoans, algae and fungi. Topics relating to viruses, viroids and prions also belong here.
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I am doing a take home exam, and there are few questions I am having trouble with answering properly.
The first question is, I have an answer somewhat but I don't know the exact reason why retroviruses cause latent infections. Can someone help me. 1. Discuss why some retroviruses cause latent infections.
Retroviruses are known to belong to the viral family Retroviriadie. They are enveloped viruses possessing an RNA genome, and replicate via a DNA intermediate. Retroviruses rely on the enzyme reverse transcriptase to perform the reverse transcription of its genome from RNA into DNA, which can then be integrated into the host's genome with an enzyme. The virus then replicates as part of the cell's DNA. Infectious retroviruses have the following criteria: generation of cells that escape a cell mediated immune response, down regulation of MHC production in infected cells so they are unable to recognized and destroyed by T-cells, and infection in cells in immunoprovlidged sites.
In latent infections, overt dieases are not produced due to the fact that viruses are dormant but at the same time the dieases are not eradicated. Latency results in a virus being able to reactivate itself while also begin able to produce large amounts of viral progeny. Amounts of viral progency is able to be produced without the host being infected by a new outside virus. Retroviruses, such as Gammaretroviruses and Episilonretroviruses appear particularly best suited for persistent infections. Retroviruses appear to persist because the virus does not disrupt the essential functions of the cells (DNA, RNA and protein synthesis). Some persistently infected cells may be assisted by the capacity of humoral Abs to cap viral Ags on the cell surface. This promotes the shredding of viral Ags from the cell surface, leaving the cell surface free of viral glycoprotein and thus the infected cell is protected from CTLs and K cells. Some retroviruses may become undetectable following a primary infection only to reappear and produce acute disease. This latency can be accomplished in different ways through development of RNA and DNA synthesis of latent infections.
The secodn question is below, I am not sure why picornaviruses are not oncogenic, just sort of guessed. 2.Explain why picornaviruses are not oncogenic tumor viruses.
In regards to tumor viruses, these viruses result from a disruption of normal restraints on cellular proliferation. There are two classes of genes that are altered expression can lead to loss of growth control. One class being stimulatory for growth which cause cancer cell hyperactivity; mutations in these genes are dominant and called oncogenes. The other class of genes that categorized with tumor viruses are anti-oncogenes. It is found that in these genes, the inhibition of cell growth which causes cancer is turned off; mutations in these genes are less dominant than oncogenes. Oncogenes being forgein, and can be carried into a cell and cause it to take on new properties such as immortalization. An example of a tumor virus, an RNA- tumor virus to be exact, are those called Retroviruses ( Kindt, pg 93).
Picornaviruses come from the Picronaviradie family. Within, this family there is a large number of viruses that can infect humans as well as animals and also amongst the smallest viruses. Picronviruses are able to withstand long periods of time sewage, water, and foods. Picornaviruses generally are not phased by antibiotics or disinfectants and can be frozen without having an effect on its function. Generally picornaviruses can be found in human tissue and can be inactivated through chlorination. Retroviruses are known to have three structural genes in its genome: gag pol and env; these genes are not oncogenic. In the case of a virus wanting to transform a cell it must have sequences that can alter cellular DNA synthesis and provide the other functions that are typical to transformed cell.
Oncogene come into play, when viral genome of many retroviruses that transform cells. An oncogenic gene in retroviruses is the sarcoma gene, deletions or even mutations in the src gene demolish transformation and tumor promotion. Other than src, there are many other types of oncogenes. Overall, Picornaviruses are small RNA viruses and are positive strand, they are not tumor causing viruses like retroviruses.
Picornaviruses do not have a DNA phase and do not cause transformation but they also cause acute infections, which are infections that develop in a given amount of time. The genomic structure and organization of picornavirues are small icosahedral with 23 capsomeres and a single messenger genome (6-10 genes). Capsid promoters consist of four polypeptides known as Viral Proteins (VP1, VP2, VP3, and VP4). These structural proteins are known to be the major building blocks of the capsid.
VP polypeptides originate from one protomer which is known as VP0 and results in different capsid components ( Rogers, pg 65).
The short answer is that picornaviurses haven’t developed any means to transform or immortalize cells because there is no advantage to the virus to do so. Picornaviruses have no DNA intermediate in their replication cycle, nor do they need much from their host beyond its nucleotide pool, charged tRNAs, ribosomes, and a suitable cell-surface receptor for viral entry. Picornaviruses have a strictly lytic growth cycle. There is no necessity to transform its host into an immortal cell—that cell is going to die after successful infection whether it is transformed/immortal or not, so why “waste” the evolutionary effort it would take to transform its host? What would be the advantage to the virus to transform a host cell into something with enhanced growth potential if the cell is only going to die sooner rather than later after the infection?
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