Poliovirus: Difference between revisions

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==Cell structure and metabolism==
==Cell structure and metabolism==
[[Image:Poliovirus_life_cycle.png|550 px|]]
[[Image:Poliovirus_life_cycle.png|580 px|]]


The cellular life cycle of poliovirus. It is initiated by binding of a poliovirion to the cell surface macromolecule CD155, which functions as the receptor (1). Uncoating of the viral RNA is mediated by receptor-dependent destabilization of the virus capsid (2). Cleavage of the viral protein VPg is performed by a cellular phosphodiesterase, and translation of the viral RNA occurs by a cap-independent (IRES-mediated) mechanism (3). Proteolytic processing of the viral polyprotein yields mature structural and non-structural proteins (4). The positive-sense RNA serves as template for complementary negative-strand synthesis, thereby producing a double-stranded RNA (replicative form, RF) (5). Initiation of many positive strands from a single negative strand produces the partially single-stranded replicative intermediate (RI) (6). The newly synthesized positive-sense RNA molecules can serve as templates for translation (7) or associate with capsid precursors to undergo encapsidation and induce the maturation cleavage of VP0 (8), which ultimately generates progeny virions. Lysis of the infected cell results in release of infectious progeny virions (9).
The cellular life cycle of poliovirus. It is initiated by binding of a poliovirion to the cell surface macromolecule CD155, which functions as the receptor (1). Uncoating of the viral RNA is mediated by receptor-dependent destabilization of the virus capsid (2). Cleavage of the viral protein VPg is performed by a cellular phosphodiesterase, and translation of the viral RNA occurs by a cap-independent (IRES-mediated) mechanism (3). Proteolytic processing of the viral polyprotein yields mature structural and non-structural proteins (4). The positive-sense RNA serves as template for complementary negative-strand synthesis, thereby producing a double-stranded RNA (replicative form, RF) (5). Initiation of many positive strands from a single negative strand produces the partially single-stranded replicative intermediate (RI) (6). The newly synthesized positive-sense RNA molecules can serve as templates for translation (7) or associate with capsid precursors to undergo encapsidation and induce the maturation cleavage of VP0 (8), which ultimately generates progeny virions. Lysis of the infected cell results in release of infectious progeny virions (9).

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Polio EM PHIL 1875 lores.png
Poliovirus
Virus classification
Group: ssRNA viruses IV
Family: Picornaviridae
Genus: Enterovirus
Sero complex: Poliovirus

Description and significance

Poliovirus was first isolated by Karl Landersteiner and Erwin Popper in 1909. Polioviruses are enteroviruses which are RNA viruses that are stable and survive in acidic conditions.

Describe the appearance, habitat, etc. of the organism, and why it is important enough to have its genome sequenced. Describe how and where it was isolated. Include a picture or two (with sources) if you can find them.

Poliovirus

Genome structure

Poliovirus is made up of a RNA genome and a protein capsid. The genome is a linear, single-stranded, positive-strand RNA and it is approximately 7,500 nucleotides long. The viral component is about 300 Angstrom in diameter with icosahdral symmetry. Poliovirus is commonly known as the most important and basic virus because of its short genome and simple composition.


Describe the size and content of the genome. How many chromosomes? Circular or linear? Other interesting features? What is known about its sequence? Does it have any plasmids? Are they important to the organism's lifestyle?

Cell structure and metabolism

Poliovirus life cycle.png

The cellular life cycle of poliovirus. It is initiated by binding of a poliovirion to the cell surface macromolecule CD155, which functions as the receptor (1). Uncoating of the viral RNA is mediated by receptor-dependent destabilization of the virus capsid (2). Cleavage of the viral protein VPg is performed by a cellular phosphodiesterase, and translation of the viral RNA occurs by a cap-independent (IRES-mediated) mechanism (3). Proteolytic processing of the viral polyprotein yields mature structural and non-structural proteins (4). The positive-sense RNA serves as template for complementary negative-strand synthesis, thereby producing a double-stranded RNA (replicative form, RF) (5). Initiation of many positive strands from a single negative strand produces the partially single-stranded replicative intermediate (RI) (6). The newly synthesized positive-sense RNA molecules can serve as templates for translation (7) or associate with capsid precursors to undergo encapsidation and induce the maturation cleavage of VP0 (8), which ultimately generates progeny virions. Lysis of the infected cell results in release of infectious progeny virions (9). [1]

Ecology

Describe any interactions with other organisms (included eukaryotes), contributions to the environment, effect on environment, etc.


Pathology

Poliovirus causes the viral disease, poliomyelitis. Poliomyelitis is an extremely infectious disease. Humans are the exclusive natural host for poliovirus. It cannot naturally infect other species. The virus takes over the nervous system and cause paralysis in hours. Poliovirus enters the body through the mouth and replicates in the throat and intestine. Once the virus remains stable in the intestine, it can enter the blood stream and pass onto the central nervous system.

As poliovirus replicates, it damages motor neurons which control the muscles for swallowing, circulation, respiration, and the trunk, arms, and legs. The damage of the motor neurons are irreversible and can cause a condition known as acute flaccid paralysis (AFP) which affects the limbs. Paralysis involving the trunk and muscles of the thorax and abdomen can result in quadriplegia. For bulbar polio, a more severe case of polio, poliovirus attacks the motor neurons of the brain stem which cause difficulty in swallowing and speaking. Without respiratory support, bulbar polio can lead to death. In the 1940s and 50s, people infected with polio that affected their respiratory muscles were immobilized in "iron lungs" - metal cylinders that were worked like a pair of bellows to regulate breathing and keep them alive. Today the iron lung has been replaced by a positive pressure ventilator.

In countries with poor sanitation, poliovirus can be spread to others by faeces of people who are infected by the virus. It can also infect vaccinated people; they will not develop polio, but can carry this virus in their gastrointestinal tract and pass it on to others.

Symptoms of individuals who are infected include fever, headache, vomitting, stiffness in the neck and pain in the back and neck. Poliovirus can also lead to paralysis, usually in the legs. Some people infected with this virus do not have any symptoms and aren't aware they have been infected.

There is no known cure for poliomyelitis.

How does this organism cause disease? Human, animal, plant hosts? Virulence factors, as well as patient symptoms.

Application to Biotechnology

Does this organism produce any useful compounds or enzymes? What are they and how are they used?


Current Research

References

http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&id=138953&lvl=3&p=cdd&p=taxonomy&lin=f&keep=1&srchmode=1&unlock

http://en.wikipedia.org/wiki/Poliovirus

http://www.ncbi.nlm.nih.gov/ICTVdb/ICTVdB/00.052.0.01.001.htm

http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?lvl=0&id=12080

http://www.ncbi.nlm.nih.gov/pubmed/10618373

http://query.nytimes.com/gst/fullpage.html?sec=health&res=9A03E2D81739F933A1575AC0A963948260

http://www.sciencemag.org/cgi/content/abstract/229/4720/1358

http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1490301