Rotavirus: Difference between revisions
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{{Curated}} | |||
{{Viral Biorealm Genus}} | |||
==Baltimore Classification== | ==Baltimore Classification== | ||
===Higher order taxa:=== | ===Higher order taxa:=== | ||
Virus; Reoviridae | Virus; dsRNA viruses; [[Reoviridae]]; ''Rotavirus'' | ||
===Species=== | ===Species=== | ||
''Rotavirus A'', ''Rotavirus B'', ''Rotavirus C'', [http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Tree&id=101358&lvl=3&lin=f&keep=1&srchmode=1&unlock unclassified Rotaviruses] | |||
==Description and Significance== | ==Description and Significance== | ||
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Rotavirus infects children at a young age but older infants and young children tend to be more symptomatic with diarrhea. There is a possibility that young infants are protected because of trans-placental transfer of antibody. In adults, asymptomatic infections are common. | Rotavirus infects children at a young age but older infants and young children tend to be more symptomatic with diarrhea. There is a possibility that young infants are protected because of trans-placental transfer of antibody. In adults, asymptomatic infections are common. | ||
Rotavirus spreads mainly from person to person via faecal-oral route and through | Rotavirus spreads mainly from person to person via faecal-oral route and through fomites. Food and water may also spread the virus while speculations have been made regarding the spread of the virus through the respiratory route. | ||
==Genome Structure== | ==Genome Structure== | ||
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==Virion Structure of a Rotavirus== | ==Virion Structure of a Rotavirus== | ||
The virions of a rotavirus consist of a capsid | The virions of a rotavirus consist of a capsid, a core, and a nucleoprotein complex. Virions loose the sometimes observed intracellular envelop during the extracellular phase during the life cycle. The virus capsid is usually not enveloped but may be enveloped when immature particles are budding into the endoplasmic reticulum, acquiring a transient lipid envelope before leaving the infected cell or not enveloped when released from the host cell as a mature virion. The capsid is round, exhibits icosahedral symmetry (T=13) and isometric with a diameter of 80 nm. The capsid shells of virions are composed of two layers. The outer shell is often lost during preparation. The capsids appear round and the surface structure is smooth, revealing a regular pattern that appears like a wheel and has distinctive features. The capsomer arrangement is clearly visible in cryoelectron microscopy. The capsid consists of 132 capsomers for both inner and outer capsids. The 132 channels are superimposed and extend inward from the surface to the core. The inner capsids consist of a rough cell and they have a diameter of about 50 nm. The core is spherical with a diameter of 35 nm. (From [http://www.ncbi.nlm.nih.gov/ICTVdb/ICTVdB/ ICTV dB Descriptions]) | ||
==Reproductive Cycle of a Rotavirus in a Host Cell== | ==Reproductive Cycle of a Rotavirus in a Host Cell== | ||
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The rotavirus replicates in the cytoplasm of the host cell. Virions enter the host cell by endocytosis and viral mRNA is transcribed using the viral RNA polymerase that is already present in the virion to form structural protein units of the capsid. The mRNA segments are assembled into the immature capsid and then replicated to form the double stranded RNA genome. | The rotavirus replicates in the cytoplasm of the host cell. Virions enter the host cell by endocytosis and viral mRNA is transcribed using the viral RNA polymerase that is already present in the virion to form structural protein units of the capsid. The mRNA segments are assembled into the immature capsid and then replicated to form the double stranded RNA genome. | ||
During the replication, rotavirus ligands on the outer capsid hemagglitinating protein VP4 bind to sialic acid receptors on the cell about to be infected. A cleavage of VP4 by trypsin is required for the virion to enter the cytoplasm, the site of rotavirus replication. This occurs when the virion makes direct contact with the cytoplasm. The rough endoplasmic reticulum retains the outer capsid lycoprotein VP7. With the help of a nonstructural glycoprotein, the rotavirus precursor buds off into the cisternae of the rough endoplasmic reticulum and acquires a temporary envelope which is later removed so that the entire outer capsid can be | During the replication, rotavirus ligands on the outer capsid hemagglitinating protein VP4 bind to sialic acid receptors on the cell about to be infected. A cleavage of VP4 by trypsin is required for the virion to enter the cytoplasm, the site of rotavirus replication. This occurs when the virion makes direct contact with the cytoplasm. The rough endoplasmic reticulum retains the outer capsid lycoprotein VP7. With the help of a nonstructural glycoprotein, the rotavirus precursor buds off into the cisternae of the rough endoplasmic reticulum and acquires a temporary envelope which is later removed so that the entire outer capsid can be assembled by VP7. The inclusion bodies are formed 6-7 hours after infection in infected cells. | ||
==Viral Ecology & Pathology== | ==Viral Ecology & Pathology== | ||
The rotavirus has infected people worldwide, causing | The rotavirus has infected people worldwide, causing 600,000-850,000 deaths each year. | ||
Various seroprevalence studies have shown that | Various seroprevalence studies have shown that antibodies are present in most infants by the age of 3. In the US, there are 20-40 deaths and about 50,000 people are hospitalized each year because of rotavirus infection. | ||
The affected host cells are mature enterocytes lining the middle and upper end of the intestinal villi. Hepatocytes are also infected in laboratory animals. It is thought that the intermediate sub-viral particle (ISVP) is the infectious particle. The viral attachment protein is probably exposed after protease digestion in the GI tract removes some or all of the outer capsid VP4. Large amounts of viral particles are shed in diarrheal stools. | The affected host cells are mature enterocytes lining the middle and upper end of the intestinal villi. Hepatocytes are also infected in laboratory animals. It is thought that the intermediate sub-viral particle (ISVP) is the infectious particle. The viral attachment protein is probably exposed after protease digestion in the GI tract and removes some or all of the outer capsid VP4. Large amounts of viral particles are shed in diarrheal stools. | ||
Histopathology of infected intestines shows villous atrophy and blunting because of the death of the mature enterocytes and infiltration of lamina propria with mononuclear cells. There is subsequently a repopulation of the villous tips with immature secretory cells. The watery diarrhea is a result of a net secretion of intestinal fluid because of the dysfunction and death of the cell. It may also be induced by the activation of the enteric nervous system. Repopulation with immature secretory cells may contribute to the secondary lactose intolerance that is sometimes observed. (From [http://pathmicro.med.sc.edu/virol/rotaviruses.htm University of South Carolina: Department of Pathology, Microbiology and Immunology]) | Histopathology of infected intestines shows villous atrophy and blunting because of the death of the mature enterocytes and infiltration of lamina propria with mononuclear cells. There is subsequently a repopulation of the villous tips with immature secretory cells. The watery diarrhea is a result of a net secretion of intestinal fluid because of the dysfunction and death of the cell. It may also be induced by the activation of the enteric nervous system. Repopulation with immature secretory cells may contribute to the secondary lactose intolerance that is sometimes observed. (From [http://pathmicro.med.sc.edu/virol/rotaviruses.htm University of South Carolina: Department of Pathology, Microbiology and Immunology]) | ||
Latest revision as of 01:18, 17 December 2010
A Viral Biorealm page on the genus Rotavirus
Baltimore Classification
Higher order taxa:
Virus; dsRNA viruses; Reoviridae; Rotavirus
Species
Rotavirus A, Rotavirus B, Rotavirus C, unclassified Rotaviruses
Description and Significance
The rotavirus is stable in the environment and is relatively resistant to handwashing agents.
Rotavirus infects children at a young age but older infants and young children tend to be more symptomatic with diarrhea. There is a possibility that young infants are protected because of trans-placental transfer of antibody. In adults, asymptomatic infections are common.
Rotavirus spreads mainly from person to person via faecal-oral route and through fomites. Food and water may also spread the virus while speculations have been made regarding the spread of the virus through the respiratory route.
Genome Structure
The genome of the rotavirus is segmented and consists of eleven segments of linear double-stranded RNA. The complete genome is 16500-21000 nucleotides long. The 5'-terminal sequence has conserved regions; 5'-end of the genome has a methylated nucleotide cap. The cap sequence type is m7G5ppp5'GmpNp. The 5'-terminus does not have a ploy (C) tract. The 3'-terminus has conserved nucleotide sequences and each sequence has conserved regions. The multipartite genome is divided among different particles, each segment encapsidated separately. Each virion contains a single, usually full length, copy of the genome. (From ICTV dB Descriptions)
Virion Structure of a Rotavirus
The virions of a rotavirus consist of a capsid, a core, and a nucleoprotein complex. Virions loose the sometimes observed intracellular envelop during the extracellular phase during the life cycle. The virus capsid is usually not enveloped but may be enveloped when immature particles are budding into the endoplasmic reticulum, acquiring a transient lipid envelope before leaving the infected cell or not enveloped when released from the host cell as a mature virion. The capsid is round, exhibits icosahedral symmetry (T=13) and isometric with a diameter of 80 nm. The capsid shells of virions are composed of two layers. The outer shell is often lost during preparation. The capsids appear round and the surface structure is smooth, revealing a regular pattern that appears like a wheel and has distinctive features. The capsomer arrangement is clearly visible in cryoelectron microscopy. The capsid consists of 132 capsomers for both inner and outer capsids. The 132 channels are superimposed and extend inward from the surface to the core. The inner capsids consist of a rough cell and they have a diameter of about 50 nm. The core is spherical with a diameter of 35 nm. (From ICTV dB Descriptions)
Reproductive Cycle of a Rotavirus in a Host Cell
The rotavirus replicates in the cytoplasm of the host cell. Virions enter the host cell by endocytosis and viral mRNA is transcribed using the viral RNA polymerase that is already present in the virion to form structural protein units of the capsid. The mRNA segments are assembled into the immature capsid and then replicated to form the double stranded RNA genome.
During the replication, rotavirus ligands on the outer capsid hemagglitinating protein VP4 bind to sialic acid receptors on the cell about to be infected. A cleavage of VP4 by trypsin is required for the virion to enter the cytoplasm, the site of rotavirus replication. This occurs when the virion makes direct contact with the cytoplasm. The rough endoplasmic reticulum retains the outer capsid lycoprotein VP7. With the help of a nonstructural glycoprotein, the rotavirus precursor buds off into the cisternae of the rough endoplasmic reticulum and acquires a temporary envelope which is later removed so that the entire outer capsid can be assembled by VP7. The inclusion bodies are formed 6-7 hours after infection in infected cells.
Viral Ecology & Pathology
The rotavirus has infected people worldwide, causing 600,000-850,000 deaths each year.
Various seroprevalence studies have shown that antibodies are present in most infants by the age of 3. In the US, there are 20-40 deaths and about 50,000 people are hospitalized each year because of rotavirus infection.
The affected host cells are mature enterocytes lining the middle and upper end of the intestinal villi. Hepatocytes are also infected in laboratory animals. It is thought that the intermediate sub-viral particle (ISVP) is the infectious particle. The viral attachment protein is probably exposed after protease digestion in the GI tract and removes some or all of the outer capsid VP4. Large amounts of viral particles are shed in diarrheal stools.
Histopathology of infected intestines shows villous atrophy and blunting because of the death of the mature enterocytes and infiltration of lamina propria with mononuclear cells. There is subsequently a repopulation of the villous tips with immature secretory cells. The watery diarrhea is a result of a net secretion of intestinal fluid because of the dysfunction and death of the cell. It may also be induced by the activation of the enteric nervous system. Repopulation with immature secretory cells may contribute to the secondary lactose intolerance that is sometimes observed. (From University of South Carolina: Department of Pathology, Microbiology and Immunology)
References
CDC
University of South Carolina: Department of Pathology, Microbiology and Immunology
