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PubMed1999

Comparison between RT-PCR and rapid agglutination test for diagnosis of human rotavirus infection.

Rotavirus represents the major cause of dehydrating diarrhea among infants and young children on worldwide scale and has recently become the target of research aimed at developing a vaccine. To that end, screening tests of clinical specimens ought to provide high sensitivity and specificity. Hence, in order to achieve that aim we compared a commercially available latex agglutination (LA) kit with reverse transcription polymerase chain reaction (RT-PCR) using primers amplifying the gene for the major neutralization antigen in 71 stool samples of children with acute gastroenteritis during November 1998-April 1999. Based on accuracy (76.05%), specificity (86.8%) and sensitivity (63.6%) determined for LA with RT-PCR serving as the gold standard, we recommend LA for field studies where speed and simplicity are crucial. Yet, for the purpose of further studies as to epidemiology and vaccine trials RT-PCR with its higher specificity and sensitivity will be required.

Cost-Benefit Analysis↗
PubMed1991

Murine intestinal antibody response to heterologous rotavirus infection.

Rotavirus is the most important worldwide cause of severe gastroenteritis. Extensive efforts have been devoted to the design of a vaccine that will prevent disease, but development of a more effective vaccine strategy may require progress in the understanding of the mucosal immune response to replicating viral antigens. In this article, we report the characterization of the intestinal antibody response of a murine model to heterologous infection with the rhesus rotavirus vaccine strain. We have adapted the enzyme-linked immunospot assay to measure this response without the difficulties associated with measurement of antibodies in intestinal contents or the artifacts associated with culturing of lymphocytes. The predominant response in terms of antibody-secreting cells (ASC) is seen in the small intestine lamina propria, which can be measured within 4 days of infection, peaks 3 weeks after infection, and remains near that level for longer than 8 weeks. The magnitude of the immunoglobulin A (IgA) cell response is approximately 10 times greater than the intestinal IgG cell response, and IgM cells are rare. Virus-specific ASC constitute approximately 50% of all ASC in the gut at the peak of the virus-specific response. This response is considerably greater than responses to nonreplicating mucosal antigens measured by similar techniques. Enteral infection engenders minimal virus-specific ASC response in the spleen. Rhesus rotavirus-specific enzyme-linked immunosorbent assay and neutralization assays of serum and intestinal contents did not correlate with virus-specific ASC response.

Animals↗
PubMed2006

Redundant role of chemokines CCL25/TECK and CCL28/MEC in IgA+ plasmablast recruitment to the intestinal lamina propria after rotavirus infection.

Rotaviruses (RV) are the most important cause of severe childhood diarrheal disease. In suckling mice, infection with RV results in an increase in total and virus-specific IgA(+) plasmablasts in the small intestinal lamina propria (LP) soon after infection, providing a unique opportunity to study the mechanism of IgA(+) cell recruitment into the small intestine. In this study, we show that the increase in total and RV-specific IgA(+) plasmablasts in the LP after RV infection can be blocked by the combined administration of Abs against chemokines CCL25 and CCL28, but not by the administration of either Ab alone. RV infection in CCR9 knockout mice still induced a significant accumulation of IgA(+) plasmablasts in the LP, which was blocked by the addition of anti-CCL28 Ab, confirming the synergistic role of CCL25 and CCL28. The absence of IgA(+) plasmablast accumulation in LP following combined anti-chemokine treatment was not due to changes in proliferation or apoptosis in these cells. We also found that coadministration of anti-CCL25 and anti-CCL28 Abs with the addition of anti-alpha(4) Ab did not further inhibit IgA(+) cell accumulation in the LP and that the CCL25 receptor, CCR9, was coexpressed with the intestinal homing receptor alpha(4)beta(7) on IgA(+) plasmablasts. Finally, we showed that RV infection was associated with an increase in both CCL25 and CCL28 in the small intestine. Hence, our findings indicate that alpha(4)beta(7) along with either CCR9 or CCR10 are sufficient for mediating the intestinal migration of IgA(+) plasmablasts during RV infection.

Animals↗
PubMed1990

Rotavirus infection and rotavirus serum antibody in a cohort of children from Gaza observed from birth to the age of one year.

Rotaviruses were studied in a cohort of children from Gaza, during their first year of life. Surveillance was effected through visits to the local health clinic by parents and infants, and to a lesser extent, field workers' home visits. The observed rate of diarrhoea (all causes), and of rotavirus-associated diarrhoea was 1.25 and 0.1 episode per child-year, respectively. Of the 130 diarrhoea episodes in the cohort, only 6.9% were rotavirus-associated. Only nine (37.5%) of 24 children in whom rotavirus antigen was detected experienced a bout of diarrhoeal illness. However, 59.2% of cohort children had rotavirus serum antibodies by one year of age. The data indicate that rotavirus excretion in Gazan children tends to be asymptomatic during the first year of life.

Antibodies, Viral↗
PubMed1990

[Comparison of clinical features of rotavirus infection with rotavirus antigen titers in feces obtained during the acute phase].

When fecal specimens obtained from infants with acute gastroenteritis during the acute phase between January 1986 and March 1987 were examined by enzyme immunoassay (EIA), 72 cases were found to have the rotavirus antigen. Such 3 clinical signs as diarrhea (D), fever (F) and vomiting (V) were all observed in 38 cases. These cases showing DFV syndrome demonstrated the highest geometric mean titer of rotavirus antigen among the rotavirus antigen-positive cases. Geometric mean titers (GMTs) were calculated to be as high as more than 10(3.1) in 26 of the 38 DFV cases (68%) and in 11 of 34 cases with DV, DF, FV or D syndromes (32%), showing a significant difference between the 2 groups (p less than 0.005). GTMs were slightly higher in cases having fever of 38 degrees C or more, than in those having fever of less than 38 degrees C.

Acute Disease↗
PubMed1981

[Incidence of rotavirus infection and in combined infection of rotavirus and enteropathogenic Escherichia coli in French calves (author's transl)].

Detection of a rotavirus in faeces of 789 calves developing diarrhoea gave positive results among 48% of the calves. The same investigation extended to 96 apparently healthy animals shows that 12.5% of the faeces contained rotavirus. It appears that all the last ones cannot be considered as healthy controls. Association of rotavirus and E. coli K99+ is found in 5% of sick animals less than 10 days old.

Age Factors↗
PubMed2006

Active viremia in rotavirus-infected mice.

Rotavirus circulates extraintestinally in animals used as models for rotavirus infection and in children. Rotavirus infection in mice was used to define host or viral factors that affect rotavirus viremia. Antigenemia was observed with homologous and heterologous rotaviruses, and neither age nor mouse strain genetics altered the occurrence of rotavirus antigenemia or viremia. Rotavirus RNA and infectious virus were present in sera and associated with the plasma fraction of blood in all infected mice. These findings indicate that antigenemia/viremia occurs routinely in rotavirus infections and imply that infectious rotavirus has access to any extraintestinal cell within contact of blood.

Animals↗
PubMed1996

Rotavirus infection in infants as protection against subsequent infections.

BACKGROUND: Rotavirus is the leading cause of severe diarrhea in infants. To provide a base line for assessing the efficacy of rotavirus vaccines, we evaluated the protection that is conferred by natural rotavirus infection. METHODS: We monitored 200 Mexican infants from birth to two years of age by weekly home visits and stool collections. A physician assessed the severity of any episodes of diarrhea and collected additional stool specimens for testing by enzyme immunoassay and typing of strains. Serum collected during the first week of life and every four months thereafter was tested for antirotavirus IgA and IgG. RESULTS: A total of 316 rotavirus infections were detected on the basis of the fecal excretion of virus (56 percent) or a serologic response (77 percent), of which 52 percent were first and 48 percent repeated infections. Children with one, two, or three previous infections had progressively lower risks of both subsequent rotavirus infection (adjusted relative risk, 0.62, 0.40, and 0.34, respectively) and diarrhea (adjusted relative risk, 0.23, 0.17, and 0.08) than children who had no previous infections. No child had moderate-to-severe diarrhea after two infections, whether symptomatic or asymptomatic. Subsequent infections were significantly less severe than first infections (P=0.024), and second infections were more likely to be caused by another G type (P=0.054). CONCLUSION: In infants, natural rotavirus infection confers protection against subsequent infection. This protection increases with each new infection and reduces the severity of the diarrhea.

Antibodies, Bacterial↗
PubMed1992

The effect of dexamethasone-induced immunosuppression on the development of faecal antibody and recovery from and resistance to rotavirus infection.

Rotavirus-naive and rotavirus-immune gnotobiotic calves were treated with high doses of dexamethasone (DX) to suppress the immune system. Calves were then infected with a virulent rotavirus inoculum, J-160, to investigate the role of immune responses both in recovery from primary rotavirus infection and in resistance to secondary rotavirus infection. Treatment of calves with DX markedly suppressed in vitro responsiveness of peripheral blood lymphocytes to mitogens within 48 h of the start of DX treatment. Suppression was similar in rotavirus-naive and rotavirus-immune calves. In contrast, the effect of DX treatment on specific antibody responses differed depending on when DX treatment started in relation to rotavirus infection. When DX treatment commenced prior to primary rotavirus infection both systemic and local specific antibody responses were inhibited. These calves, in which mitogen and antibody responses were suppressed, exhibited greater clinical signs than did control calves after infection with virulent rotavirus, but virus excretion was affected in only one of the two calves. When DX treatment was started after primary rotavirus infection but before secondary infection, systemic and local antibody responses to the primary infection and to the challenge infection were not affected. These calves resisted challenge with virulent virus as did DX-untreated rotavirus-immune calves, even though mitogen responses were suppressed. We conclude that in a primary rotavirus infection, virus excretion ceased when both antibody and mitogen responses were suppressed. Resistance to secondary rotavirus infection occurred when mitogen responsiveness was suppressed, but when antibody levels were normal. Thus, no evidence was obtained that fully functional cell-mediated immune mechanisms are essential for resistance to rotavirus infection. Evidence was provided for the ability of parenteral treatment with DX to suppress mucosal as well as systemic antibody responses.

Animals↗
PubMed1993

Protection conferred by neonatal rotavirus infection against subsequent rotavirus diarrhea.

A cohort of newborns in New Delhi who were nosocomially infected with rotavirus during their first days of life were followed twice weekly for 14-23 months to determine whether neonatal infection protected them against subsequent episodes of rotavirus diarrhea. Infection occurred in 60% by the fourth day of life, was asymptomatic, and was caused predominantly by an unusual rotavirus strain (G9 P11) not previously identified in humans. The 148 children with neonatal rotavirus infection had 46% fewer attacks of rotavirus diarrhea in the follow-up period than the 56 infants without nosocomial infection (0.23 vs. 0.42 episodes/child-year, P < .05). This protection was concentrated among infants in their first year of life and was not associated with a significant decrease in disease severity. Consideration of this strain as a vaccine candidate will require further assessment of its natural protection under field conditions.

Cohort Studies↗
PubMed2002

Group A rotavirus infection and age-dependent diarrheal disease in rats: a new animal model to study the pathophysiology of rotavirus infection.

Group A rotaviruses are major pathogens causing acute gastroenteritis in children and animals. To determine if group A rotavirus replicates and induces disease in rats, antibody-negative Lewis neonatal or adult rats were inoculated orally with tissue culture-adapted human (Wa, WI61, and HAL1166), simian (rhesus rotavirus [RRV] and SA11), bovine (WC3), lapine (ALA), or porcine (OSU) rotavirus strains, wild-type murine (EC(wt)) rotavirus strain, or phosphate-buffered saline (PBS). Rotavirus infection in rats was evaluated by (i) clinical findings, (ii) virus antigen shedding or infectious virus titers in the feces or intestinal contents measured by enzyme-linked immunosorbent assay or fluorescent-focus assay, (iii) histopathological changes in the small intestine, (iv) distribution of rotavirus antigen in small-intestine sections by immunofluorescence, and (v) growth rate. Rotavirus infection of 5-day-old but not > or =21-day-old rats resulted in diarrhea that lasted from 1 to 10 days postinoculation. The severity of disease and spread of infection to naIve littermates differed depending on the virus strain used for inoculation. The duration of virus antigen shedding following infection was considerably prolonged (up to 10 days) in neonatal rats compared to that in 21-day-old rats (1 or 2 days). Based on lack of virus antigen shedding and disease induction, the murine EC(wt) rotavirus was the only strain tested that did not infect rats. Histopathological changes in the small-intestine mucosa of 5-day-old RRV-inoculated rats but not of PBS-inoculated rats was limited to extensive enterocyte vacuolation in the ileum. In RRV-inoculated neonatal rats, rotavirus antigen was detected in the epithelial cells on the upper half of the intestinal villi of the jejunum and ileum. In addition, infection of neonatal rats with RRV but not with PBS resulted in reduced weight gain. Rats infected with group A rotaviruses provide a new animal model with unique features amenable to investigate rotavirus pathogenesis and the molecular mechanisms of intestinal development, including physiological factors that may regulate age-dependent rotavirus-induced diarrhea.

Age Factors↗
PubMed1998

Rotavirus infection and rates of hospitalisation for acute gastroenteritis in young children in Australia, 1993-1996.

OBJECTIVE: To determine rates of hospitalisation of young children for acute gastroenteritis in Australia, and to estimate the proportion of these admissions caused by rotavirus infection. DESIGN: Analysis of hospital admission records, and parallel, prospectively collected data on rotavirus-positive admissions. SETTING: Hospitals admitting young children in all Australian States and Territories in 1993-1996. PATIENTS: All children under five years admitted to hospital for acute gastroenteritis (International Classification of Diseases, ninth revision principal diagnosis codes 003.0, 004.0-009.3 and 558.9). MAIN OUTCOME MEASURES: Rate of hospital admission per 1000 children per year by State, and the proportion of admissions caused by rotavirus infection. RESULTS: There were almost 20,000 hospital admissions annually in Australia for acute gastroenteritis in children under five years, at an average rate of 15/1000. An estimated 50% of these were attributable to rotavirus infection, implying a rate of hospitalisation for rotavirus-related gastroenteritis of 7.5/1000/year. Among children under two years this rate was 11.6/1000. Rotavirus incidence rates generally followed a typical seasonal pattern in temperate regions of the country, with sharp peaks in mid to late winter. Rates of hospitalisation varied markedly, even between States with apparently similar patterns of disease, while the incidence in the Northern Territory was 3-5 times higher than other States. CONCLUSIONS: Rotavirus-related gastroenteritis is a major cause of hospital admissions in young children, and large savings to the healthcare system are possible if it can be prevented at reasonable cost. Variation in treatment practices between States may be worth studying in greater detail as another source of potential savings.

Acute Disease↗
PubMed1994

High prevalence of rotavirus infection among neonates born at hospitals in Delhi, India: predisposition of newborns for infection with unusual rotavirus.

Although rotavirus is the most common cause of diarrhea in children older than 3 months of age, neonatal infections, which are asymptomatic, have rarely been surveyed and have been identified in only a few discrete nosocomial outbreaks. After such a nosocomial outbreak of rotavirus infection among newborns at a hospital in Delhi, we screened infants born at five other nurseries in the immediate area to assess the prevalence of neonatal infections and to determine whether the unique neonatal rotavirus strain, 116E, previously identified in Delhi, was present in other settings. Infection was documented in 43 to 78% of hospitalized infants between 4 and 6 days of life born at five of the six hospitals. Infection with strains related to 116E were the most common, but other unusual strains and no strains common in the community were detected. In addition a shift in genotype was observed among specimens collected from two of these hospitals during a 2-year period. Our observation that neonatal rotavirus infections are more common than recognized previously would encourage the administration of rotavirus vaccines during the newborn period and suggests that the low efficacy of vaccines observed during trials in developing countries may be caused by early natural exposure of infants before immunization. The extraordinary predisposition of neonates for unusual rotavirus strains not commonly found in the community should encourage others to screen neonates for this infection, characterize the strains more fully and attempt to understand at a molecular level the unique relationship between the infecting strain type and the age of the host.

Feces↗
PubMed2004

Rotavirus infection in adults.

Rotavirus has been recognised for 30 years as the most common cause of infectious gastroenteritis in infants and young children. By contrast, the role of rotavirus as a pathogen in adults has long been underappreciated. Spread by faecal-oral transmission, rotavirus infection in adults typically manifests with nausea, malaise, headache, abdominal cramping, diarrhoea, and fever. Infection can also be symptomless. Rotavirus infection in immunocompromised adults can have a variable course from symptomless to severe and sustained infection. Common epidemiological settings for rotavirus infection among adults include endemic disease, epidemic outbreak, travel-related infection, and disease resulting from child-to-adult transmission. Limited diagnostic and therapeutic alternatives are available for adults with suspected rotavirus infection. Because symptoms are generally self-limiting, supportive care is the rule. Clinicians caring for adults with gastroenteritis should consider rotavirus in the differential diagnosis. In this review we intend to familiarise clinicians who primarily provide care for adult patients with the salient features of rotavirus pathophysiology, clinical presentation, epidemiology, treatment, and prevention.

Adult↗
PubMed1981

Acute diarrhea and rotavirus infection in newborn babies and children in Yogyakarta, Indonesia, from June 1978 to June 1979.

A longitudinal study of acute diarrhea in children in Yogyakarta, Indonesia (June 1978 to June 1979), showed little variation throughout most months of the year in numbers of children admitted to hospital and in numbers infected with rotaviruses. Both decreased during November and December coincidentally with seasonal change from dry to wet conditions. Rotavirus particles were identified by electron microscopy in fecal specimens from 126 of 334 (38%) infants and children with acute diarrhea. Nosocomial rotavirus infections occurred in 11% of control children admitted to hospital for other reasons. Socioeconomic level and preexisting nutritional status did not influence the incidence of rotavirus excretion. Rotavirus infections were most common in children aged 6 to 24 months. There was a low incidence of infection in infants less than 6 months old. Rotavirus infection was seldom observed in newborn babies delivered in an urban hospital nursery, in a rural health center, or at home. One of 72 newborn babies with diarrhea excreted rotavirus. One of 53 healthy newborn babies excreted rotavirus. It is concluded that, in Indonesia, rotavirus infection is a major cause of childhood diarrhea throughout the year, but is an uncommon cause of diarrhea in newborn babies.

Age Factors↗
PubMed2005

Homeostasis and function of goblet cells during rotavirus infection in mice.

Rotaviruses are the leading cause of severe viral gastroenteritis in young children. To gain insight in goblet cell homeostasis and intestinal mucin expression during rotavirus infection, 6-day-old mice were inoculated with murine rotavirus. To determine epithelial cell migration, mice were injected with BrdU just before inoculation. Small intestines were isolated at different days postinfection (dpi) and evaluated for rotavirus and goblet cell-specific gene expression. Small intestinal mucins of control and infected animals at 1, 2, and 4 dpi were isolated and tested for their capability to neutralize rotavirus infection in vitro. After inoculation, two peaks of viral replication were observed at 1 and 4 dpi. During infection, the number of goblet cells in infected mice was decreased in duodenum and jejunum, but was unaffected in the ileum. Goblet cells in infected animals accumulated at the tips of the villi. Muc2 mRNA levels were increased during the peak of viral replication at 1 dpi, whereas at other time points Muc2 and Tff3 mRNA levels were maintained at control levels. Muc2 protein levels in the tissue were also maintained, however Tff3 protein levels were strongly decreased. The number of goblet cells containing sulfated mucins was reduced during the two peaks of infection. Mucins isolated at 1 and 2 dpi from control and infected mice efficiently neutralized rotavirus infection in vitro. Moreover, mucins isolated from infected mice at 4 dpi were more potent in inhibiting rotavirus infection than mucins from control mice at 4 dpi. In conclusion, these data show that during rotavirus infection, goblet cells, in contrast to enterocytes, are relatively spared from apoptosis especially in the ileum. Goblet cell-specific Muc2 expression is increased and mucin structure is modified in the course of infection. This suggests that goblet cells and mucins play a role in the active defense against rotavirus infection and that age-dependent differences in mucin quantities, composition, and/or structure alter the anti-viral capabilities of small intestinal mucins.

Animals↗
PubMed1990

Effect of rotavirus infection and malnutrition on uptake of a dietary antigen in the intestine.

Intestinal absorption of ovalbumin (OVA), a dietary macromolecule, was studied in malnourished and normally nourished suckling mice after experimentally induced infection with rotavirus. All mice developed diarrhea within 24 to 48 h postinoculation. The malnourished animals exhibited more severe symptoms and an increased number of rotavirus-containing enterocytes in intestinal sections as compared to well-nourished mice when examined 3 d postinoculation, at the peak of diarrhea. Histopathologic examination revealed villus atrophy and pronounced vacuolization of villus enterocytes in association with malnutrition and rotavirus infection. The combination of malnutrition and viral infection resulted in more severe mucosal damage, including disruption of microvillus borders. After a single oral dose of 100 micrograms OVA at 3 d postinoculation, the concentration of OVA in serum, gastric content, intestinal lavage fluid, and intestinal tissue homogenates was measured at different time intervals. The concentrations of OVA in intestinal tissue were significantly higher in malnourished animals, whereas lower values were found in rotavirus-infected animals. In all mice, OVA was rapidly absorbed and could be consistently detected in the serum within 5 min. OVA levels peaked at 45 to 60 min and then gradually declined. In malnourished infected animals, the uptake of OVA was rapid and resulted in significantly higher serum levels when compared to well nourished or uninfected controls, respectively. The peak uptake of OVA per g body wt was about 4.5 times more in malnourished infected compared to well-nourished infected mice and 2.5 times higher in normally nourished infected animals when compared to uninfected controls. These results indicate that rotavirus infection in association with malnutrition may cause a significant rise in gut permeability to environmental macromolecules.

Animals↗