Download 10 Chapter 37 Reo Calici

Reoviruses,
Rotaviruses and
Caliciviruses
Chapter 37
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Properties of Reoviruses
Structure
Icosahedral, 60-80 nm, double
capsid shell
Segmented, double-stranded
RNA; 16-27 kb
9 structural proteins, several
enzymes packaged in virus
Nonenveloped
Cytoplasmic replication
Extremely stable
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Heat resistant
Remain infectious after treatment of
pH 3-9
Classification
Respiratory, enteric, orphan
Family Reoviridae
Nine genera
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Reovirus Replication
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Receptor-mediated attachment and endocytosis
Vesicle is targeted to lysosome (fusion)
Drop in pH allows virus to shed its outer capsid
This results in inner capsid escape into the cytoplasm
The RNA transcriptase (a polymerase) is activated
Inner capsid uncoats, releasing RNAs into cytoplasm
Viral mRNA synthesis is initiated
Viral polypeptides are synthesized
A viral replicase synthesizes second RNA strand
Assembly occurs in cytoplasm
Mature virus exits when cell dies from lysis
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Rotaviruses
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Major cause of diarrhea
Similar to reoviruses in morphology and replication strategy
Classification
Five serological groups (A-E)
Group A can be distinguished from others by electophoretic
mobility of gene segments
Animal susceptibility
Rotaviruses are highly promiscuous
Major cause of disease in livestock industry
Many young animals can become persistent carriers, shedding
virus to other animals
Difficult to propagate in cell culture systems
Often requires infection of animals, then harvesting virus from
diarrhea
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Rotavirus Gene Segments
Segmen
Product
t
Location
Function
1
VP1
Inner core
RNA polymerase
2
VP2
Inner core
RNA-binding protein
3
VP3
Inner core
Guanyltransferase
4
VP4
Outer capsid
HA, neutralizing antigen, protease, cell attachment
5
NSP1
Nonstructural
RNA-binding zinc finger protein (transcription factor)
6
VP6
Inner capsid
Trimer, hydrophobic
7
NSP3
Nonstructural
RNA-binding protein
8
NSP2
Nonstructural
RNA-binding protein
9
VP7
Outer capsid
RER integral membrane protein
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NSP4
Nonstructural
RER integral membrane protein
11
NSP5
Nonstructural
RNA-binding
Rotavirus Pathogenesis
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Infect villi of small intestine
Multiply in enterocytes
Distrupts cellular transport systems
Endoplasmic reticulum in particular
Damaged cells slough off and shed virus
Enterocytes are replaced by crypt cells
Crypt cells have different sodium and glucose transport
features that lead to fluid loss in the small intestine
Diarrhea ensues
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Rotavirus Pathogenesis
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Clinical findings and laboratory diagnosis
Principally a disease of children
Can be fatal if not treated (hydration)
Diagnostic by ELISA or PCR
Epidemiology and Immunity
3 to 5 billion cases per year
As many as 5 million deaths
50% of childhood gastroenteritis are caused by rotaviruses
IgA controls infection and provides immunity of differential
durability
Treatment and control
Treatment is replacement of fluids and electrolytes
Vaccine licensed in US in 1998 but was withdrawn because of
bowel obstructions in some children
New vaccine has recently been approved
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Caliciviruses
Gastroenteritis
Norwalk virus and Norwalk-like viruses
Recently infamous for cruise ship infections
Extremely difficult to decontaminate
Unculturable (propagated in animals)
Family Caliciviridae
Clinical Findings and Laboratory Diagnosis
Diarrhea
No defined demographic distribution
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In the absence of bacterial etiology, such diarrheal disease is presumed a
calicivirus
Diagnosic is by PCR
Epidemiology and Immunity
Clustered outbreaks
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Food and water-borne
Communicable
Immunity is not durable
Other Reoviradae Members
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Orbiviruses
Naturally infect insects
Can be transmitted to vertebrates
Problem in livestock industries
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Bluetongue virus of sheep
African horse sickness
Astroviruses
Single-stranded plus sense RNA
Diarrhea
Children and institutionalized elderly
Can establish persistent infection in immunocompromised
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