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Sapporo Virus: History and Recent Findings
Shunzo Chiba, Shuji Nakata,
Kazuko Numata-Kinoshita, and Shinjiro Honma
Department of Pediatrics, Sapporo Medical University
School of Medicine, Sapporo, Japan
Morphologically distinct caliciviruses of human origin were first found in stools of children
with gastroenteritis in 1976. Sapporo virus, or human calicivirus Sapporo, with typical surface
morphology was first detected during a gastroenteritis outbreak in a home for infants in
Sapporo, Japan, in 1977. Since then, morphologically and antigenically identical virus has
been detected frequently in the same institution in association with outbreaks of gastroenteritis. Sapporo virus is widely distributed worldwide, as evidenced by the appearance of
antigenically or genetically similar viruses and seroepidemiologic findings. Sapporo virus plays
an important role in outbreaks of infantile gastroenteritis and is less important in foodborne
outbreaks. Sapporo virus has been approved as the type species of the genus “Sapporo-like
viruses” in the family Caliciviridae. The history of and recent findings, as obtained by newly
developed techniques, about Sapporo viruses are presented.
Since calicivirus was first discovered as a causative agent of
vesicular exanthema of swine and later found in various wild
and domestic animals, studies of this group of viruses have
been done primarily in the field of veterinary medicine [1, 2].
In 1976, after the introduction of direct electron microscopy
(EM), Madeley and Cosgrove [3] and Flewett and Davies [4]
were the first to find morphologically typical caliciviruses of
human origin in the stools of children with gastroenteritis. Over
the next few years, sporadic cases and outbreaks of gastroenteritis associated with morphologically typical caliciviruses were
reported from Norway [5], the United Kingdom [6], Canada
[7], and Japan [8–10]. Studies of gastroenteritis outbreaks in
London [11–13] and Sapporo [8, 14, 15] have provided convincing evidence that these viruses can cause gastroenteritis in
people of all ages.
Sapporo virus (SV) was first named after its discovery in an
outbreak of gastroenteritis in a home for infants in Sapporo,
Japan, in October 1977 [8]. Morphologically similar viruses
were detected in a subsequent series of outbreaks in the same
institution between 1977 and 1982. They have a typical “Starof-David” configuration by EM (figure 1) and are antigenically
identical to each other by immune EM (IEM). In collaboration
with others, we have conducted extensive studies based on the
stool materials collected in these early outbreaks.
The inability to propagate SV and Norwalk virus (NV) in
cell culture or animal models hampered progress in the research
on this group of viruses. However, recent success in cloning the
NV genome [16] initiated a molecular phase of calicivirus research in humans. On the basis of extensive worldwide genetic
Reprints or correspondence: Prof. Shunzo Chiba, Dept. of Pediatrics,
Sapporo Medical University School of Medicine, S1, W16, Chuo-ku, Sapporo, 060-8543, Japan.
The Journal of Infectious Diseases 2000; 181(Suppl 2):S303–8
q 2000 by the Infectious Diseases Society of America. All rights reserved.
0022-1899/2000/18105S-0011$02.00
analysis, most of the small round structured viruses (SRSVs),
or Norwalk-like viruses, are now included in the family Caliciviridae [16–18]. On the other hand, the “classical human caliciviruses,” with typical calicivirus morphology, also have been
proven genetically to be members of the Caliciviridae [19, 20].
Caliciviruses in animals and in humans are now classified
into 4 genera [18]: Vesivirus (represented by swine vesicular
exanthema virus and feline calicivirus), Lagovirus (represented
by rabbit hemorrhagic disease virus and European brown hare
syndrome virus), “Norwalk-like virus” (represented by NV),
and “Sapporo-like viruses” (represented by SV). The latter 2
genera are provisionally named. NV is divided into 2 genogroups: GI (represented by NV 68 [prototype of NV]) and GII
(represented by Snow Mountain virus). These genogroups are
further divided into many clusters on the basis of sequence
differences of the RNA-dependent RNA polymerase and capsid
protein regions of the genomes [21]. SV is proposed to be divided into at least 3 genogroups [17, 22, 23]: Sapporo virus 82
(SV82), a prototype of SV, genogroup (including Manchester
virus [19] and Houston/86 [24]), London 92 genogroup (including Pretoria 92 and Pretoria 94), and Parkville virus genogroup (including Houston/90 strain).
Herein, we describe the discovery and early studies of SV by
EM and IEM, and we describe some recent findings on the
virology, genetic and antigenic classification, and epidemiology
of SV.
Discovery of SV and Earlier Studies by EM and IEM
Information essential to our knowledge of SV was gained by
earlier EM and IEM studies of virus associated with gastroenteritis outbreaks that occurred in the Sapporo infant home
in October 1977 and August 1979 [8, 14, 15, 25]. The home
had 93 residents (1–27 months old) during the outbreaks. Of
these 93 infants, 77 (83%) had gastrointestinal symptoms, including diarrhea (73, 95%), vomiting (34, 44%), and fever (14,
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Chiba et al.
Figure 1.
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Sapporo virus particles in fecal extract. Star-of-David configuration is apparent.
18%). The home has four separate rooms, in which infants are
housed according to age. The outbreaks moved in sequence
from room to room, suggesting spread by person-to-person
contact (figure 2) [15].
EM examination of fecal specimens from the infants revealed
typical calicivirus particles. Of 61 specimens examined, 29 (48%)
contained calicivirus particles. A relationship between fecal
shedding of virus and the day of illness was clearly demonstrated [14]. No virus was found in stool samples obtained from
children before the onset of illness; however, virus was found
in 95% of stool samples collected within 4 days after the onset
of illness and in 50% of samples collected during the next 5
days. Thereafter, calicivirus was detected rarely in stool specimens. IEM tests for antibody responses against one of the
isolated virus strains were done on paired pre-illness and convalescent sera derived from the first outbreak. Seroconversion
was demonstrated in 95% of affected infants and in 75% of
unaffected infants, indicating subclinical infection in these children [8, 15].
On the basis of the IEM test results, the virus appeared to
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Sapporo Virus: History and Recent Findings
have no antigenic relationship to the following 5 candidate
viruses for gastroenteritis: NV, Hawaii agent, W agent, Otofuke
agent, and unclassified small round virus-like particles (table
1). Serum specimens from children and adults living in Sapporo
were tested for antibody against SV by IEM (figure 3). The
results suggested that infection with SV is common, beginning
in infancy and increasing during early childhood [25].
Virologic and Genetic Characteristics of SV
Studies of the virologic and genetic nature of SV have been
done using viruses derived from two outbreaks that occurred
in 1981 and 1982. The 1982 virus strain (SV82) has been extensively studied and became a prototype strain of SV. Viral
particles in the stools of a patient with gastroenteritis were
purified, radiolabeled, and analyzed by SDS–polyacrylamide
gel electrophoresis. A single major structural protein with a
molecular mass of 62,000 daltons was identified by immunoprecipitation [26]. This finding is consistent with SV being a
member of the family Caliciviridae.
Phylogenetic analysis of the sequences of RNA polymerase
regions showed that SV82 is closer to animal caliciviruses than
to other known human caliciviruses [27]. The nonstructural and
capsid protein coding sequences in the SV82 genome are fused
in a single open-reading frame. This genome organization is
similar to that of rabbit hemorrhagic disease virus and the
recently described Manchester virus, and they are distinct from
that of NV 68 and other SRSVs lacking typical calicivirus morphology [19, 20]. Expression of the capsid protein of SV82 in
insect cells resulted in the self-assembly of virus-like particles
that are morphologically similar to the native virus [20].
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Table 1. Antigenic comparison of the Sapporo virus with 5 other
agents by immune electron microscopy (IEM).
Serum samples
Calicivirus (patient)
Before illness
Convalescence
Norwalk agent (chimpanzee)
Before inoculation
After inoculation
Hawaii agent (volunteer)
Before inoculation
After inoculation
W agent (volunteer)
Before inoculation
After inoculation
Small round virus-like particles (patient)
Acute phase
Convalescence
Otofuke agent (patient)
Acute phase
Convalescence
Calicivirus
0
41
0
0
0
0
11
11
0
0
31
31
NOTE. Values represent IEM antibody scores of paired sera from individual
humans and animals infected with various viruses and agents when tested against
Sapporo virus. Data adapted from [15].
Immunologic Aspects of SV
SV is antigenically distinct from NV as determined on the
basis of IEM results [15]. By radioimmunoassay (RIA), using
antigens prepared from fecal samples, SV was shown to be
antigenically different from NV and some strains of morphologically typical calicivirus found in the United Kingdom [28].
More recently, molecular characterization of NV and SV has
led to the development of an enzyme immunoassays (EIAs)
that use recombinant baculovirus-expressed capsid proteins to
detect calicivirus antigens and antibodies [29, 30]. The results
Figure 2. Distribution of patients according to date of illness onset in two outbreaks of acute gastroenteritis. A, First outbreak. B, Second
outbreak. Groups A–D are age groups: A = <6 months old, B = 7–12 months old, C = 13–18 months old, D = 19–24 months old. Reprinted
with permission from [15].
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Chiba et al.
JID 2000;181 (Suppl 2)
virus correlates with protection from clinical illness following
reinfection with the virus. It remains unclear, however, whether
serum antibody is of primary importance in resistance to SV
gastroenteritis or if it mirrors the antibody response in the gut
[28].
Evidence for the Worldwide Prevalence of SV
Figure 3. Age-related immune electron microscopy (IEM) antibody
scores to Sapporo virus. Closed and open circles represent antibodypositive and -negative samples, respectively. m = months; y = years.
Reprinted with permission from Wiley-Liss, Inc., a subsidiary of John
Wiley & Sons, Inc., from [25].
of these new EIAs clearly showed that NV/GI, NV/GII, and
SV also correspond to distinct antigenic groups [30].
To assess humoral immunity in infants with SV gastroenteritis, we used RIA-blocking tests to analyze paired samples of
pre- and post-outbreak sera from patients and healthy contacts
involved in an outbreak at the Sapporo infant home [31]. Of
41 residents, 18 had pre-existing serum antibody to human
calicivirus (titers 11 : 50) and 23 did not, as determined by RIA.
Three of the 18 infants with antibody became ill, compared
with 18 of the 23 without antibody (P ! .01 by x2 analysis) [31].
These results suggest that antibody responses to SV follow
typical primary and secondary (or booster) responses to common human viral illnesses. In individuals lacking pre-existing
antibody to the virus, antibody titers rose rapidly after infection
and were maintained at the same level or at slightly elevated
levels 3 months after infection. On the other hand, individuals
with pre-existing antibody showed a sharp rise in antibody titers
1 month after infection and a decline in titers 3 months after
infection. The presence of pre-existing serum antibody to the
The evidence of worldwide distribution of SV was based on
detection of SV and antibody prevalence against SV in different
populations around the world. SV was initially detected in 1977
in an infant home in Sapporo. Between 1977 and 1982, there
were three more gastroenteritis outbreaks in the home. Virus
strains associated with the four outbreaks all showed a typical
Star-of-David configuration by EM, and they were antigenically identical by IEM, RIA, or EIA. SV has also been detected
by the use of immunoassay, reverse transcription–polymerase
chain reaction (RT-PCR), or sequence analysis in other areas
of Japan [32] and in the United States [24, 33], United Kingdom
[19], Saudi Arabia (Cubitt WD, personal communication),
South Africa [34], Kenya [35], Australia [36], and Finland [37].
The virus has been circulating in Sapporo for 120 years since
its discovery [32] (unpublished data).
Seroepidemiologic studies have shown a worldwide distribution of this virus, including Japan, the United States, the
United Kingdom, Canada, China, Kenya, and Southeast Asia
[32, 35, 38, 39]. SV has been detected mainly in infants and
younger children. The age-related prevalence of antibody
against this virus also has shown that infections commonly
occur in children !5 years old [25, 35, 39]. The pattern of acquisition of the antibody is similar to that of other common
virus infections, including rotavirus infection. The pattern of
acquisition of antibodies to NV are shifted to older children
and adults [29, 35, 40].
Thus, SV is thought to be a common cause of viral gastroenteritis in infants and young children worldwide, but it appears
to be less common as a cause of severe diarrhea and hospitalization. The virus has been detected rarely in association with
foodborne outbreaks. However, the use of sensitive assay systems (e.g., RT-PCR) has made it easier than previously possible
to detect SV in stools from younger patients.
Importance of NV and SV As Causes of Gastroenteritis
Outbreaks among Infants
We have done a long-term study on the causative agents of
outbreaks of gastroenteritis in a home for infants where SV
was first discovered in association with gastroenteritis in 1977.
From 1976 to 1995, 36 outbreaks of nonbacterial gastroenteritis
have occurred in this orphanage, which houses otherwise
healthy homeless infants. Diarrheal stool samples obtained during the outbreaks were examined for gastroenteritis viruses by
EM, EIA, or RT-PCR for group A rotaviruses, enteric adenoviruses, astroviruses, NV, and SV. Isolates of SV and NV
JID 2000;181 (Suppl 2)
Sapporo Virus: History and Recent Findings
were further tested by Southern hybridization and sequencing
of PCR products.
Data from the first 10 years of study were previously summarized [41]. We performed EM examinations of stool specimens derived from 18 outbreaks and detected viruses or viruslike particles in all but 1 outbreak. Caliciviruses with typical
surface morphology were associated with 5 of the 18 outbreaks;
they were the second most prevalent virus after group A rotaviruses (figure 4).
We used advanced techniques, including RT-PCR, to examine stool specimens from the 36 gastroenteritis outbreaks
that occurred between 1976 and 1995. NV and SV were associated with 15 (42%) of the 36 outbreaks, and group A rotaviruses were associated with 10 (28%). Six outbreaks were
caused by SV/SV82 genogroup, 6 were caused by NV/GII, 1
was caused by a mixed infection of NV/GII and SV/SV82, and
the remaining 2 were caused by uncharacterized NV. Adenovirus and astrovirus were detected in 3 (8%) and 2 (6%), respectively, of the 36 outbreaks [42]
Outbreaks of NV and SV gastroenteritis in the Sapporo orphanage occurred almost every year, with no clear seasonal
pattern of occurrence. In contrast, gastroenteritis outbreaks due
to group A rotaviruses occurred between October and April,
mostly from December to March [42]. Thus, members of the
family Calciviridae, NV and SV, were the most common cause
of viral gastroenteritis outbreaks among infants in Sapporo,
and they were more prevalent than group A rotaviruses. The
use of recently developed molecular techniques has improved
the detection rate of NV and SV. Our choice of the primer pairs
and preparation of the specific probes for SV elucidated the
clinical importance of these viruses in infants [42].
There has been a discrepancy between the high prevalence
of antibody to NV and SV and the low detection rate of their
antigens in sporadic and outbreak cases of gastroenteritis
among children [35, 40, 43, 44]. Several possibilities have been
raised to explain this discrepancy. It may be that stool samples
have not been examined for viruses because NV- and SV-associated gastroenteritis is often too mild to require a visit to a
clinic, or it could be that practical detection methods for a
broader range of theses viruses is not available.
Our findings indicate that the number of NV- and SV-associated gastroenteritis cases among infants may be underestimated because of the lack of adequate detection methods for
these viruses, especially for SV. Reexamination by RT-PCR or
EIAs of stool samples collected in various surveys for SV may
be worthwhile, especially for the samples collected from
children.
Future Perspectives
Further studies should be done with the following in mind:
First, the relative clinical importance of SV-associated disease
burden in children must be further clarified. Second, the finding
that SV is genetically closer to animal caliciviruses than to NV
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Figure 4. Frequency of viruses associated with 18 outbreaks of gastroenteritis in an orphanage in Sapporo, 1976–1985. HRV = human
rotavirus; HCV = human calicivirus (Sapporo virus); ADV = adenovirus; SA = Sapporo agent; OAL = Otofuke agent–like; ASV = astrovirus; SRV = small round virus. Reprinted with permission from John
Wiley & Sons, Ltd., from [41].
suggests that similar diseases may occur in animals and humans
and that animal-to-human transmission is possible. Further
investigations are needed from this point of view. Third, more
extensive attempts should be made to propagate the virus in
vitro and to passage it in tissue culture.
Acknowledgments
We thank M. K. Estes (Division of Molecular Virology, Baylor College of Medicine, Houston) and X. Jiang and D. O. Matson (Center
for Pediatric Research, Children’s Hospital of the King’s Daughters,
Eastern Virginia Medical School, Norfolk, VA) for their continued
collaboration and contribution to the studies reviewed in this article.
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