Reoviruses,Rotaviruses, & Caliciviruses

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Reoviruses, Rotaviruses,
& Caliciviruses
Reoviruses are medium-sized viruses with a doublestranded,
segmented RNA genome. The family includes
human rotaviruses, the most important cause of infantile
gastroenteritis around the world (Figure 37–1).
Acute gastroenteritis is a very common disease with significant
public health impact. In developing countries it
is estimated to cause as many as 3.5 million deaths of
preschool children annually. In the United States, acute
gastroenteritis is second only to acute respiratory infections
as a cause of disease in families.
Caliciviruses are small viruses with a single-stranded
RNA genome. The family contains Norwalk virus, the
major cause of nonbacterial epidemic gastroenteritis
worldwide.
PROPERTIES OF REOVIRUSES
Important properties of reoviruses are summarized in
Table 37–1.
Structure & Composition
The virions measure 60–80 nm in diameter and possess
two concentric capsid shells, each of which is icosahedral.
(Rotaviruses have a triple-layered structure.)
Rotaviruses have 132 capsomeres; there is no envelope.
Single-shelled virus particles that lack the outer capsid
are 50–60 nm in diameter. The inner core of the particles
is 33–40 nm in diameter (Figure 37–2). The double-shelled
particle is the complete infectious form of
the virus.
The genome consists of double-stranded RNA in
10–12 discrete segments with a total genome size of
16–27 kbp, depending on the genus. Rotaviruses contain
11 genome segments, whereas orthoreoviruses and
orbiviruses each possess ten segments and coltiviruses
have 12 segments. The individual RNA segments vary
in size from 680 bp (rotavirus) to 3900 bp (orthoreovirus).
The virion core contains several enzymes
needed for transcription and capping of viral RNAs.
Reoviruses are unusually stable to heat, to a 3.0–9.0
range of pH, and to lipid solvents, but they are inacti-
504
37
vated by 95% ethanol, phenol, and chlorine. Limited
treatment with proteolytic enzymes increases infectivity.
Classification
The family Reoviridae is divided into nine genera. Four
of the genera are able to infect humans and animals:
Orthoreovirus, Rotavirus, Coltivirus, and Orbivirus. Four
other genera infect only plants and insects, and one
infects fish.
There are at least three major subgroups and nine
serotypes of human rotaviruses. Strains of human and
animal origin may fall in the same serotype. Five other
serotypes are found only in animals. Three different
serotypes of reovirus are recognized, along with about 100
different orbivirus serotypes and two coltivirus serotypes.
Reovirus Replication
Viral particles attach to specific receptors on the cell surface
(Figure 37–3). The cell attachment protein for
reoviruses is the viral hemagglutinin (σ1 protein), a
minor component of the outer capsid.
After attachment and penetration, uncoating of virus
particles occurs in lysosomes in the cell cytoplasm. Only
the outer shell of the virus is removed, and a core-associated
RNA transcriptase is activated. This transcriptase
transcribes mRNA molecules from the minus strand of
each genome double-stranded RNA segment contained
in the intact core. The functional mRNA molecules correspond
in size to the genome segments. Reovirus cores
contain all enzymes necessary for transcribing, capping,
and extruding the mRNAs from the core, leaving the
double-stranded RNA genome segments inside.
Once extruded from the core, the mRNAs are translated
into primary gene products. Some of the fulllength
transcripts are encapsidated to form immature
virus particles. A viral replicase is responsible for synthesizing
negative-sense strands to form the doublestranded
genome segments. This replication to form
progeny double-stranded RNA occurs in partially completed
core structures. The mechanisms that ensure

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Unknown
Bacteria
Adenovirus
Astrovirus
Calicivirus
Rotavirus
assembly of the correct complement of genome segments
into a developing viral core are unknown. Viral
polypeptides probably self-assemble to form the inner
and outer capsid shells.
Reoviruses produce inclusion bodies in the cytoplasm
in which virus particles are found. These viral factories
are closely associated with tubular structures
(microtubules and intermediate filaments). Rotavirus
morphogenesis involves budding of single-shelled particles
into the rough endoplasmic reticulum. The “pseudoenvelopes”
so acquired are then removed and the
outer capsids are added (Figure 37–3). This unusual
pathway is utilized because the major outer capsid protein
is glycosylated.
Cell lysis results in release of progeny virions.
ROTAVIRUSES
Rotaviruses are a major cause of diarrheal illness in
human infants and young animals, including calves and
REOVIRUSES, ROTAVIRUSES, & CALICIVIRUSES / 505
Unknown
Parasites
Other bacteria
Toxigenic
Escherichia coli
Astrovirus
Adenovirus
Calicivirus
Developed countries Developing countries
Rotavirus
Figure 37–1. An estimate of the role of etiologic agents in severe diarrheal illnesses requiring hospitalization of
infants and young children in developed countries (left) and in developing countries (right). (Reproduced, with permission,
from Kapikian AZ: Viral gastroenteritis. JAMA 1993;269:627.)
Table 37–1. Important properties of reoviruses.
Virion: Icosahedral, 60–80 nm in diameter, double capsid shell
Composition: RNA (15%), protein (85%)
Genome: Double-stranded RNA, linear, segmented (10–12
segments); total genome size 16–27 kbp
Proteins: Nine structural proteins; core contains several
enzymes
Envelope: None (transient pseudoenvelope is present
during rotavirus particle morphogenesis)
Replication: Cytoplasm; virions not completely uncoated
Outstanding characteristics:
Genetic reassortment occurs readily
Rotaviruses are the major cause of infantile diarrhea
Reoviruses are good models for molecular studies of viral
pathogenesis
piglets. Infections in adult humans and animals are also
common. Among rotaviruses are the agents of human
infantile diarrhea, Nebraska calf diarrhea, epizootic
diarrhea of infant mice, and SA11 virus of monkeys.
Rotaviruses resemble reoviruses in terms of morphology
and strategy of replication.
Figure 37–2. Electron micrograph of a negatively
stained preparation of human rotavirus. (D, doubleshelled
particles; S, single-shelled particles; E, empty
capsids; i, fragment of inner shell; io, fragments of a
combination of inner and outer shell.) Inset: Singleshelled
particles obtained by treatment of the viral
preparation with sodium dodecyl sulfate. Bars, 50 nm.
(Courtesy of J Esparza and F Gil.)

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506 / CHAPTER 37
Viroplasm VP1,2,3,6
NSP2,5
Double-shelled virus
Cell
lysis
RER
Nucleus
Transient enveloped
particle
Envelope
removal
Classification & Antigenic Properties
Rotaviruses have been classified into five groups (A–E)
based on antigenic epitopes on the internal structural
protein VP6. These can be detected by immunofluorescence,
ELISA, and immune electron microscopy (IEM).
Group A rotaviruses are the most frequent human
pathogens. Outer capsid proteins VP4 and VP7 carry epitopes
important in neutralizing activity, with VP7 glycoprotein
being the predominant antigen. These typespecific
antigens differentiate among rotaviruses and are
demonstrable by Nt tests. Multiple serotypes have been
identified among human and animal rotaviruses. Some
animal and human rotaviruses share serotype specificity.
For example, monkey virus SA11 is antigenically very
similar to human serotype 3. The gene-coding assignments
responsible for the structural and antigenic specificities
of rotavirus proteins are shown in Figure 37–4.
?
Assembly of single-shelled particles
?
Ca 2+
Progeny virions
Lysosome
VP4
?
NSP
7M G
7M G
Translation
VP1,2,3,4,6,7
NSP1,2,3,5
RER
Molecular epidemiologic studies have analyzed isolates
based on differences in the migration of the 11
genome segments following electrophoresis of the RNA
in polyacrylamide gels (Figure 37–5). These differences
in electropherotypes can be used to differentiate group
A viruses from other groups, but they cannot be used to
predict serotypes.
Animal Susceptibility
Infecting virus
Single-shelled
particle
7MG 7MG 7MG 7MG NSP3
VP7
mRNA
Figure 37–3. Overview of the rotavirus replication cycle. (Reproduced, with permission, from Estes MK: Rotaviruses
and their replication. In: Fields Virology, 3rd ed. Fields BN et al [editors]. Lippincott-Raven, 1996.)
NSP4
Rotaviruses have a wide host range. Most isolates have
been recovered from newborn animals with diarrhea.
Cross-species infections can occur in experimental inoculations,
but it is not clear if they occur in nature. Swine
rotavirus infects both newborn and weanling piglets.
Newborns often exhibit subclinical infection due perhaps
to the presence of maternal antibody, whereas overt
disease is more common in weanling animals.
+
+
+
+

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RNA
segment Protein
1
2
3
4
5
6
7
8
9
10
11
Propagation in Cell Culture
Rotaviruses are fastidious agents to culture. Most group
A human rotaviruses can be cultivated if pretreated with
the proteolytic enzyme trypsin and if low levels of
trypsin are included in the tissue culture medium. This
cleaves an outer capsid protein and facilitates uncoating.
Very few non-group A rotavirus strains have been cultivated.
Pathogenesis
VP1
VP2
VP3
VP4
NSP1
VP6
NSP2
NSP3
VP7
NSP4
NSP5
Rotaviruses infect cells in the villi of the small intestine
(gastric and colonic mucosa are spared). They multiply
in the cytoplasm of enterocytes and damage their transport
mechanisms. One of the rotavirus-encoded proteins,
NSP4, is a viral enterotoxin and induces secretion
by triggering a signal transduction pathway. Damaged
cells may slough into the lumen of the intestine and
release large quantities of virus, which appear in the
stool (up to 10 10 particles per gram of feces). Viral
excretion usually lasts 2–12 days in otherwise healthy
patients but may be prolonged in those with poor nutrition.
Diarrhea caused by rotaviruses may be due to
impaired sodium and glucose absorption as damaged
cells on villi are replaced by nonabsorbing immature
REOVIRUSES, ROTAVIRUSES, & CALICIVIRUSES / 507
VP2
VP4,
neutralization
antigen
VP6,
subgroup
antigen
VP7,
neutralization
antigen
Subcore
Figure 37–4. Gene-coding assignments for antigenic specificities of rotavirus proteins. Shown on the left are the
genome RNA segments and the encoded protein products. In the center is a schematic representation of the complete
rotavirus particle with the location of the structural proteins in the different shells indicated.The figure on the
right shows the three-dimensional structure of a virus particle. A complete particle is drawn on the left half; the
structure on the right half has part of the outer and inner shells removed to show the middle and inner shells. (Reproduced
from Estes MK: Rotaviruses and their replication. In: Fields Virology, 3rd ed. Fields BN et al [editors]. Lippincott-Raven,
1996. Modified from Conner ME, Matson DO, Estes MK: Rotavirus vaccines and vaccination potential. Curr Top Microbiol
Immunol 1994;185:285, with an unpublished structure of BVV Prasad and A Shaw.)
crypt cells. It may take 3–8 weeks for normal function
to be restored.
Clinical Findings & Laboratory Diagnosis
Rotaviruses cause the major portion of diarrheal illness
in infants and children worldwide but not in adults
(Table 37–2). There is an incubation period of 1–3
days. Typical symptoms include watery diarrhea, fever,
abdominal pain, and vomiting, leading to dehydration.
In infants and children, severe loss of electrolytes and
fluids may be fatal unless treated. Patients with milder
cases have symptoms for 3–8 days and then recover
completely. However, viral excretion in the stool may
persist up to 50 days after onset of diarrhea. Asymptomatic
infections, with seroconversion, occur. In children
with immunodeficiencies, rotavirus can cause severe and
prolonged disease.
Adult contacts may be infected, as evidenced by seroconversion,
but they rarely exhibit symptoms, and virus
is infrequently detected in their stools. A common source
of infection is contact with pediatric cases. However, epidemics
of severe disease have occurred in adults, especially
in closed populations, as in a geriatric ward. Group
B rotaviruses have been implicated in large outbreaks of
severe gastroenteritis in adults in China (Table 37–2).

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Figure 37–5. Electrophoretic profiles of rotavirus RNA
segments.Viral RNAs were electrophoresed in 10%
polyacrylamide gels and visualized by silver stain. Different
rotavirus groups and RNA patterns are illustrated:
a group A monkey virus (SA11; lane A), a group A
human rotavirus (lane B), a group B human adult diarrhea
virus (lane C), and a group A rabbit virus that
exhibits a “short” RNA pattern (lane D). Rotaviruses contain
11 genome RNA segments, but sometimes two or
three segments migrate closely together and are difficult
to separate. (Photograph provided by T Tanaka and
MK Estes.)
Laboratory diagnosis rests on demonstration of virus
in stool collected early in the illness and on a rise in antibody
titer. Virus in stool is demonstrated by IEM, latex
agglutination tests, or ELISA. Genotyping of rotavirus
nucleic acid from stool specimens by the polymerase
chain reaction is the most sensitive detection method.
Serologic tests can be used to detect an antibody titer
rise, particularly ELISA.
Epidemiology & Immunity
Rotaviruses are the single most important worldwide
cause of gastroenteritis in young children. Estimates
range from 3 billion to 5 billion for annual diarrheal
episodes in children under 5 years of age in Africa, Asia,
and Latin America, resulting in as many as 5 million
deaths. Developed countries have a high morbidity rate
but a low mortality rate. Typically, up to 50% of cases of
acute gastroenteritis of hospitalized children throughout
the world are caused by rotaviruses.
Rotavirus infections usually predominate during the
winter season. Symptomatic infections are most common
in children between ages 6 months and 2 years,
and transmission appears to be by the fecal-oral route.
Nosocomial infections are frequent.
Rotaviruses are ubiquitous. By age 3 years, 90% of
children have serum antibodies to one or more types.
This high prevalence of rotavirus antibodies is maintained
in adults, suggesting subclinical reinfections by
the virus. Rotavirus reinfections are common; it has
been shown that young children can suffer up to five
reinfections by 2 years of age. Asymptomatic infections
are more common with successive reinfections. Local
immune factors, such as secretory IgA or interferon,
may be important in protection against rotavirus infection.
Asymptomatic infections are common in infants
before age 6 months, the time during which protective
maternal antibody acquired passively by newborns
should be present. Such neonatal infection does not prevent
reinfection, but it does protect against the development
of severe disease during reinfection.
Treatment & Control
Treatment of gastroenteritis is supportive, to correct the
loss of water and electrolytes that may lead to dehydration,
acidosis, shock, and death. Management consists
of replacement of fluids and restoration of electrolyte
balance either intravenously or orally, as feasible. The
infrequent mortality from infantile diarrhea in developed
countries is due to routine use of effective replacement
therapy.
In view of the fecal-oral route of transmission, wastewater
treatment and sanitation are significant control
measures.
An oral live attenuated rhesus-based rotavirus vaccine
was licensed in the United States in 1998 for vaccination
of infants. It was withdrawn a year later because of reports
of intussusception (bowel blockages) as an uncommon
but serious side effect associated with the vaccine. A safe
and effective vaccine remains the best hope for reducing
the worldwide burden of rotavirus disease.
REOVIRUSES
The viruses of this genus, which have been studied most
thoroughly by molecular biologists, are not known to
cause human disease.
Classification & Antigenic Properties
Reoviruses are ubiquitous, with a very wide host range.
Three distinct but related types of reovirus have been

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Table 37–2. Viruses associated with acute gastroenteritis in humans. 1
Important as a
Size Cause of
Virus (nm) Epidemiology Hospitalization
Rotaviruses
Group A 60–80 Single most important cause (viral or bacterial) of endemic Yes
severe diarrheal illness in infants and young children worldwide
(in cooler months in temperate climates).
Group B 60–80 Outbreaks of diarrheal illness in adults and children in China. No
Group C 60–80 Sporadic cases and occasional outbreaks of diarrheal illness
in children.
No
Enteric adenovirus
Caliciviruses
70–90 Second most important viral agent of endemic diarrheal illness
of infants and young children worldwide.
Yes
Norwalk 27–40 Important cause of outbreaks of vomiting and diarrheal illness
in older children and adults in families, communities, and
institutions; frequently associated with ingestion of food.
No
Sapporo 27–40 Sporadic cases and occasional outbreaks of diarrheal illness
in infants, young children, and the elderly.
No
Astroviruses 28–30 Sporadic cases and occasional outbreaks of diarrheal illness
in infants, young children, and the elderly.
No
1 Modified from Kapikian AZ: Viral gastroenteritis. JAMA 1993;269:627.
recovered from many species and are demonstrable by
Nt and HI tests. Reoviruses contain a hemagglutinin for
human O or bovine erythrocytes.
Epidemiology
Reoviruses cause many inapparent infections, because
most people have serum antibodies by early adulthood.
Antibodies are also present in other species. All three
types have been recovered from healthy children, from
young children during outbreaks of minor febrile illness,
from children with diarrhea or enteritis, and from
chimpanzees with epidemic rhinitis.
Human volunteer studies have failed to demonstrate
a clear cause-and-effect relationship of reoviruses to
human illness. In inoculated volunteers, reovirus is
recovered far more readily from feces than from the nose
or throat. An association of reovirus type 3 with biliary
atresia in infants has been suggested.
Pathogenesis
Reoviruses have become important model systems for
the study of the pathogenesis of viral infection at the
molecular level. Defined recombinants from two
reoviruses with differing pathogenic phenotypes are
REOVIRUSES, ROTAVIRUSES, & CALICIVIRUSES / 509
used to infect mice. Segregation analysis is then used to
associate particular features of pathogenesis with specific
viral genes and gene products. The pathogenic properties
of reoviruses are primarily determined by the protein
species found on the outer capsid of the virion.
ORBIVIRUSES
Orbiviruses are a genus within the reovirus family. They
commonly infect insects, and many are transmitted by
insects to vertebrates. About 100 serotypes are known.
None of these viruses cause serious clinical disease in
humans, but they may cause mild fevers. Serious animal
pathogens include bluetongue virus of sheep and
African horse sickness virus. Antibodies to orbiviruses
are found in many vertebrates, including humans.
The genome consists of ten segments of doublestranded
RNA, with a total genome size of 18 kbp. The
replicative cycle is similar to that of reoviruses.
Orbiviruses are sensitive to low pH, in contrast with the
general stability of other reoviruses.
CALICIVIRUSES
In addition to rotaviruses and noncultivable adenoviruses,
members of the family Caliciviridae are impor-

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510 / CHAPTER 37
tant agents of viral gastroenteritis in humans. The most
significant member is Norwalk virus. Properties of caliciviruses
are summarized in Table 37–3.
Classification & Antigenic Properties
Caliciviruses are similar to picornaviruses but are
slightly larger (27–40 nm) and contain a single major
structural protein. They exhibit a distinctive morphology
in the electron microscope (Figure 37–6). The family
Caliciviridae is divided into four genera: Norovirus,
which includes the Norwalk viruses; Sapovirus, which
includes the Sapporo-like viruses; Lagovirus, the rabbit
hemorrhagic disease virus; and Vesivirus, which includes
vesicular exanthem virus of swine, feline calicivirus, and
marine viruses found in pinnipeds, whales, and fish.
The first two genera contain human viruses that cannot
be cultured; the latter two genera contain only animal
strains that can be grown in vitro. Rabbit hemorrhagic
disease virus was introduced in 1995 in Australia as a
biologic control agent to reduce that country’s population
of wild rabbits.
Historically, the Norwalk viruses were referred to as
“small round structured viruses” based on their detection
by electron microscopy.
Human calicivirus serotypes are not defined. The
Norwalk viruses are subdivided into two genogroups.
Clinical Findings & Laboratory Diagnosis
Norwalk virus is the most important cause of epidemic
viral gastroenteritis in adults (Table 37–2). Epidemic
nonbacterial gastroenteritis is characterized by (1)
absence of bacterial pathogens; (2) gastroenteritis with
rapid onset and recovery and relatively mild systemic
signs; and (3) an epidemiologic pattern of a highly communicable
disease that spreads rapidly with no particular
predilection in terms of age or geography. Various
Table 37–3. Important properties of caliciviruses.
Virion: Icosahedral, 27–40 nm in diameter; cup-like depressions
on capsid surface
Genome: Single-stranded RNA, linear, positive-sense, nonsegmented;
7.4–8.3 kb in size; contains genome-linked protein
(VPg)
Proteins: Polypeptides cleaved from a precursor polyprotein;
capsid is composed of a single protein
Envelope: None
Replication: Cytoplasm
Outstanding characteristics:
Norwalk viruses are major cause of nonbacterial epidemic
gastroenteritis
Human viruses are noncultivable
descriptive terms have been used in reports of different
outbreaks (eg, epidemic viral gastroenteritis, viral diarrhea,
winter vomiting disease) depending on the predominant
clinical feature.
Norwalk viral gastroenteritis has an incubation period
of 24–48 hours. Onset is rapid, and the clinical course is
brief, lasting 12–60 hours; symptoms include diarrhea,
nausea, vomiting, low-grade fever, abdominal cramps,
headache, and malaise. The illness can be incapacitating
during the symptomatic phase, but hospitalization is
rarely required. Norwalk infections are more likely to
induce vomiting than those with Sapporo-like viruses.
Dehydration is the most common complication in the
young and elderly. No sequelae have been reported.
Volunteer experiments have clearly shown that the
appearance of Norwalk virus coincides with clinical illness.
Antibody develops during the illness and is usually
protective on a short-term basis against reinfection with
the same agent. Long-term immunity does not correspond
well to the presence of serum antibodies. Some
volunteers can be reinfected with the same virus after
about 2 years.
Reverse transcriptase-polymerase chain reaction is
the most widely used technique for detection of human
caliciviruses in clinical specimens (feces, vomitus) and
environmental samples (contaminated food, water).
Because of the genetic diversity among circulating
strains, the choice of polymerase chain reaction primer
pairs is very important.
Electron microscopy is frequently used to detect
virus particles in stool samples. However, Norwalk virus
particles are usually present in low concentration and
are difficult to recognize; they should be identified by
immunoelectron microscopy. ELISA immunoassays
based on recombinant virus-like particles can detect
antibody responses, with a fourfold or greater rise in
IgG antibody titer in acute and convalescent-phase sera
indicative of a recent infection. However, the necessary
reagents are not widely available, and the antigens are
not able to detect responses to all antigenic types of
Norwalk virus.
Epidemiology & Immunity
Human caliciviruses have worldwide distribution. Norwalk
viruses are the most common cause of nonbacterial
gastroenteritis in the United States, causing an estimated
23 million cases annually.
The viruses are most often associated with epidemic
outbreaks of waterborne, food-borne, and shellfish-associated
gastroenteritis. Community outbreaks can occur
in any season. All age groups can be affected. Outbreaks
occur throughout the year, with a seasonal peak during
cooler months. Most outbreaks involve food-borne or
person-to-person transmission.

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REOVIRUSES, ROTAVIRUSES, & CALICIVIRUSES / 511
Figure 37–6. Electron micrographs of virus particles found in stools of patients with gastroenteritis.These viruses
were visualized following negative staining. Specific viruses and the original magnifications of the micrographs are
as follows. A: Rotavirus (185,000 ×). B: Enteric adenovirus (234,000 ×). C: Coronavirus (249,000 ×). D: Torovirus (coronavirus)
(249,000 ×). E: Calicivirus (250,000 ×). F: Astrovirus (196,000 ×). G: Norwalk virus (calicivirus) (249,000 ×).
H: Parvovirus (249,000 ×).The electron micrographs in panels C–H were originally provided by T Flewett; panel E was
originally obtained from CR Madeley. Bars, 100 nm. (Reproduced, with permission, from Graham DY, Estes MK: Viral infections
of the intestine. Pages 566–578 in: Principles and Practice of Gastroenterology and Hepatology. Gitnick G et al [editors].
Elsevier Science Publishing Co., 1988.)

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Characteristics of Norwalk virus include a low infectious
dose (as few as 10 virus particles), relative stability
in the environment, and multiple modes of transmission.
It survives 10 ppm chlorine and heating to 60 °C;
it can be maintained in steamed oysters.
Fecal-oral spread is probably the primary means of
transmission of Norwalk virus. During a 5-year period
in the United States (1996–2000), food was implicated
in 39% of outbreaks of Norwalk gastroenteritis, personto-person
contact in 12%, and water in 3%, with the
source in 18% unknown.
Outbreaks of Norwalk gastroenteritis occur in multiple
settings. In the same 5-year period as above, 39%
occurred in restaurants, 29% in nursing homes and hospitals,
12% in schools and daycare centers, 10% in vacation
settings, including cruise ships, and 9% in other
settings.
No in vitro neutralization assay is available to study
immunity. Volunteer challenge studies have shown that
about 50% of adults are susceptible to illness. Norwalk
virus antibody is acquired later in life than rotavirus
antibody, which develops early in childhood. In developing
countries, most children have developed Norwalk
virus antibodies by 4 years of age.
Treatment & Control
Treatment is symptomatic. The low infectious dose permits
efficient transmission of the virus. Because of the
infectious nature of the stools, care should be taken in
their disposal. Effective hand washing can decrease
transmission in family or institutional settings. Careful
processing of food is important, as many food-borne
outbreaks occur. Purification of drinking water and
swimming pool water should decrease Norwalk virus
outbreaks. There is no vaccine.
ASTROVIRUSES
Astroviruses are about 28–30 nm in diameter and
exhibit a distinctive morphology in the electron microscope
(Figure 37–6). They contain single-stranded, positive-sense
RNA, 6.8–7.9 kb in size. At least eight
serotypes of human viruses are recognized by IEM and
neutralization. Astroviruses cause diarrheal illness and
may be shed in extraordinarily large quantities in feces.
Astroviruses are transmitted by the fecal-oral route
through contaminated food or water, person-to-person
contact, or contaminated surfaces. They are recognized
as pathogens for infants and children, elderly institutionalized
patients, and immunocompromised persons
(Table 37–2). They may be shed for prolonged periods
by immunocompromised hosts.
REVIEW QUESTIONS
1. A 36-year-old man enjoyed a meal of raw oysters.
Twenty-four hours later he became ill, with
sudden onset of vomiting, diarrhea, and
headache.The most likely cause of his gastroenteritis
is
(A) Astrovirus
(B) Hepatitis A virus
(C) Norwalk virus
(D) Rotavirus, group A
(E) Echovirus
2. This virus is the most important cause of gastroenteritis
in infants and young children. It
causes infections that are often severe and may
be life-threatening, especially in infants.
(A) Echovirus
(B) Norwalk virus
(C) Rotavirus, group A
(D) Orbivirus
(E) Parvovirus
3. An outbreak of epidemic gastroenteritis
occurred at a wooded summer camp 24 hours
after a party for visiting families. Some of the
visiting parents became ill also. Samples taken 2
weeks later from the well that was the source of
drinking water at the camp were negative for
fecal coliforms. The most likely source of the
outbreak was
(A) Mosquitoes or ticks, present in high numbers
in the area
(B) Contaminated food served at the party
(C) A nearby stream used for fishing
(D) A visiting parent who was developing
pneumonia
(E) The swimming pool
4. This viral gastroenteritis agent has a segmented,
double-stranded RNA genome and a doubleshelled
capsid. It is a member of which virus
family?
(A) Adenoviridae
(B) Astroviridae
(C) Caliciviridae
(D) Reoviridae
(E) Coronaviridae
5. Rotavirus and Norwalk virus are distinctly different
viruses. However, they share which one of
the following characteristics?
(A) Fecal-oral mode of transmission
(B) They mainly cause disease in infants and
young children

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(C) They induce generally mild disease in
young children
(D) Infection patterns show no seasonal variation
(E) A double-stranded RNA genome
6. Because rotavirus infections can be serious, a vaccine
would be beneficial. Which of the following
is most correct regarding a rotavirus vaccine?
(A) A killed human rotavirus group A vaccine is
in use in the United States (2003)
(B) A live attenuated vaccine was withdrawn
from use because of reports of intussusception
(1998)
(C) Vaccine development is complicated by
rapid antigenic variation by the virus
(D) Available antiviral drugs make a vaccine
unnecessary
(E) Vaccine development is complicated
because the virus cannot be grown in cell
culture
REOVIRUSES, ROTAVIRUSES, & CALICIVIRUSES / 513
Answers
1. C 4. D
2. C 5. A
3. B 6. B
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