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At least 19 recordsLinked to original sources
PubMed1999

The epithelial cell response to rotavirus infection.

Rotavirus is the most important worldwide cause of severe gastroenteritis in infants and young children. Intestinal epithelial cells are the principal targets of rotavirus infection, but the response of enterocytes to rotavirus infection is largely unknown. We determined that rotavirus infection of HT-29 intestinal epithelial cells results in prompt activation of NF-kappaB (<2 h), STAT1, and ISG F3 (3 h). Genetically inactivated rotavirus and virus-like particles assembled from baculovirus-expressed viral proteins also activated NF-kappaB. Rotavirus infection of HT-29 cells induced mRNA for several C-C and C-X-C chemokines as well as IFNs and GM-CSF. Mice infected with simian rotavirus or murine rotavirus responded similarly with the enhanced expression of a profile of C-C and C-X-C chemokines. The rotavirus-stimulated increase in chemokine mRNA was undiminished in mice lacking mast cells or lymphocytes. Rotavirus induced chemokines only in mice <15 days of age despite documented infection in older mice. Macrophage inflammatory protein-1beta and IFN-stimulated protein 10 mRNA responses occurred, but were reduced in p50-/- mice. Macrophage inflammatory protein-1beta expression during rotavirus infection localized to the intestinal epithelial cell in murine intestine. These results show that the intestinal epithelial cell is an active component of the host response to rotavirus infection.

Aging↗
PubMed2003

Central nervous system involvement in neonatal rotavirus infection.

Rotavirus is an ubiquitous virus associated with severe gastro-enteritis in children under 2 years of age. However, serious conditions, including central nervous system involvement, have been associated with rotavirus infection. We investigated the clinical signs and symptoms of rotavirus infection in 156 neonates, specifically focusing on neurological signs. Neurological signs identified were apnoea, jitteriness, convulsions and poor sucking. Of the 156 babies, 66 were rotavirus-positive and 90 rotavirus-negative. In the rotavirus-positive group, 19.7% manifested apnoea compared with 22.2% in the rotavirus-negative group. The other three symptoms occurred in <10% of the neonates. Rotavirus dsRNA was detected by RT-PCR in the CSF of two. One had apnoea, the other no CNS symptoms. Although rotavirus infection in neonates is hardly ever asymptomatic and may cause death, it has not been associated with CNS symptomatology in our studies.

Central Nervous System Viral Diseases↗
PubMed2002

Gene expression pattern in Caco-2 cells following rotavirus infection.

Rotaviruses are recognized as the leading cause of severe dehydrating diarrhea in infants and young children worldwide. Preventive and therapeutic strategies are urgently needed to fight this pathogen. In tissue culture and in vivo, rotavirus induces structural and functional alterations in the host cell. In order to better understand the molecular mechanisms involved in the events after rotavirus infection, we identified host cellular genes whose mRNA levels changed after infection. For this analysis, we used microarrays containing more than 38,000 human cDNAs to study the transcriptional response of the human intestinal cell line Caco-2 to rotavirus infection. We found that 508 genes were differentially regulated >2-fold at 16 h after rotavirus infection, and only one gene was similarly regulated at 1 h postinfection. Of these transcriptional changes, 73% corresponded to the upregulation of genes, with the majority of them occurring late, at 12 or more hours postinfection. Some of the regulated genes were classified according to known biological function and included genes encoding integral membrane proteins, interferon-regulated genes, transcriptional and translational regulators, and calcium metabolism-related genes. A new picture of global transcriptional regulation in the infected cell is presented and families of genes which may be involved in viral pathogenesis are discussed.

Animals↗
PubMed1986

T-cell-deficient mice display normal recovery from experimental rotavirus infection.

Rotaviruses are common causes of diarrhea in animals and humans. Little is known, however, about the components of the host response to these viruses. Rotavirus infection was studied in athymic mice experimentally infected with murine rotavirus. Neonatal T-cell-deficient mice experienced a self-limited gastrointestinal infection which was identical to that observed in age-matched immunocompetent mice. Adult T-cell-deficient seronegative mice and age-matched normal mice showed a similar extent of resistance to symptomatic rotavirus infection. In both cases, the infection was resolved without the generation of antirotavirus antibody. These studies indicate that host defense against murine rotavirus requires neither functional T-lymphocytes nor specific antiviral antibody.

Animals↗
PubMedDate not supplied

[The determination of human IgM rotavirus antibodies in the blood serum by an immunoenzyme method in patients with a rotavirus infection].

Rotavirus infection is one of the infectious diseases which can be verified only by a laboratory assay. That is why elaboration of new methods of the infection serodiagnosis is of great importance. Enzyme-linked immunoassay was worked up for IgM rotavirus antibodies detection in human blood serum. Validation of the method provides grounds for its being recommended for the diagnosis of rotavirus infection alongside with the determination of rotavirus antigens in feces.

Antibodies, Viral↗
PubMed2005

Viraemia is a common finding in immunocompetent children with rotavirus infection.

Rotavirus infection is usually localized to the intestine but involvement of extra-intestinal sites, including the respiratory tract, liver, kidney, lymph nodes, and central nervous system, has been reported. The extra-intestinal spread of the virus may occur through blood since viraemia has been documented occasionally in animals and humans. Nevertheless, the questions of how common viraemia is in immunocompetent children and whether it is associated with extra-intestinal manifestations remain unsolved. Serum samples from 54 immunocompetent children hospitalized for acute diarrhea were evaluated prospectively for the presence of rotavirus RNA by nested reverse transcriptase-polymerase chain reaction (RT-PCR) to investigate this issue. Rotavirus antigens were detected in the stools of 14 children. A bacterial aetiology was documented in 14 cases, and in the remaining cases the aetiology remained unknown. Rotavirus RNA was detected in the blood of 9/14 (64.3%) rotavirus infected children but in no child with diarrhea of other origin. Positive RT-PCR was associated with high fever and/or evidence of extra-intestinal involvement. All positive samples were collected within 3 days of illness onset, suggesting that viraemia was detectable for only a few days. Children in whom rotavirus was detected only in stool samples had high fever but no other extra-intestinal feature. These data suggest that viraemia is common in children infected with rotavirus, which may be associated with extra-intestinal involvement.

Antigens, Viral↗
PubMed1982

Sudden infant death syndrome associated with rotavirus infection.

Rotavirus was detected in the stools of five children stricken with sudden infant death syndrome (SIDS) over a three-week period. While none of the children had acute gastroenteritis, four of the five had acute upper respiratory infections. Rotavirus was also identified in tracheal aspirates from two of the infants. Extensive investigations failed to reveal the presence of any other viruses or toxins in specimens obtained from the five children with SIDS. Rotavirus was not found in the stool specimens obtained from a control group of 36 infants including six who died of causes other than SIDS. Future attempts at the prevention of rotavirus infections should be directed at populations susceptible to sudden infant death syndrome.

Feces↗
PubMed1994

Protection against rotavirus disease after natural rotavirus infection. US Rotavirus Vaccine Efficacy Group.

Determination of protective efficacy after natural rotavirus infection is important as a basis for evaluating rotavirus vaccines. Therefore, placebo recipients in a large 2-year rotavirus vaccine trial conducted across the United States were followed to determine the protection afforded by natural rotavirus infection. Serotype 1 rotaviruses predominated (93% year 1, 66% year 2), but isolates of all four major human rotavirus serotypes circulated during both years. Of the 45 placebo recipients with documented rotavirus illnesses in year 1, 1 developed rotavirus disease in year 2 compared with 29 of the other 235 placebo recipients (P = .03). Serologic data were available for 171 placebo recipients, and 37 of 140 without rotavirus illnesses in year 1 had evidence of asymptomatic rotavirus infection. None of these 37 experienced rotavirus disease in year 2 compared with 22 of the remaining 103 (P < .001). Overall efficacy after natural rotavirus infection was 93% (95% confidence interval, 50%-99%).

Antibodies, Viral↗
PubMed1979

Comparison of methods for immunocytochemical detection of rotavirus infections.

Rotavirus infections in intestinal tissues of animals or in tissue culture cells were detected by the immunocytochemical unlabeled soluble enzyme peroxidase antiperoxidase method. Comparison of the immunofluorescence and peroxidase antiperoxidase immunological staining techniques revealed that the two methods are equally sensitive for detection of rotavirus-infected cells. The peroxidase antiperoxidase technique offers the advantages of negligible nonspecific staining reactions, the use of a standard light microscope, the production of permanent slides, and the conservation of immunological reagents. The ability to detect antigens in paraffin-embedded tissues enhances the usefulness of the peroxidase antiperoxidase test for both prospective and retrospective studies.

Animals↗
PubMed1996

Natural history of human rotavirus infection.

Rotavirus infections occur repeatedly in humans from birth to old age. Most are asymptomatic or are associated with mild enteric symptoms. Infection in young children can be accompanied by severe life-threatening diarrhea, most commonly after primary infection. Annual childhood morbidity rates for severe diarrhea are similar worldwide. Mortality rates are low in developed countries but approach 1,000,000 annually in young children in developing countries. Rotaviruses can be classified into Groups A-E according to antigenic groups on VP6, the major capsid antigen. Only Group A,B and C rotaviruses have been shown to infect humans, and most human rotavirus disease is caused by Group A viruses. These are further classified into G and P types based on identification of antigens on the outer capsid proteins VP7 and VP4 respectively. Most severe infections in young children are caused by serotypes G1-4, and during the last two decades, G1 infections appear to have predominated worldwide. In general the more densely populated countries show the most complex patterns of occurrence of serotypes. Clinical rotavirus disease can be accompanied by shedding of > 10(12) rotavirus particles/gm feces. The virus is highly infectious and appears to retain infectivity over many months. In temperate climates, disease is most common during the colder months, when it is likely that rapid spread within families and communities occurs. Nosocomial infections are frequent, and rotaviruses can become endemic within obstetric hospital nurseries for the newborn. Few (if any) human rotavirus infections appear to be zoonoses, even though Group A rotaviruses are widespread in the young of all mammalian species. However infection of humans with reassortant rotavirus strains derived from human-animal sources can occur. The extent to which this contributes to new epidemic strains within particular countries (or worldwide) remains to be determined.

Age Factors↗
PubMedDate not supplied

Molecular biology and immunology of rotavirus infections.

Rotaviruses were first recognized about 15 years ago in association with diarrhea in children and animals. Since then, rotaviruses have been determined to be the most important viral agent that causes clinically significant diarrhea in children and a need for an effective vaccination program has been recognized. This article reviews the progress which has been made in understanding the molecular biology of rotaviruses and summarizes information on the immune responses to rotavirus infections obtained in a new animal model in rabbits. This model is useful to systematically evaluate active protective immunity following infection of seronegative animals.

Animals↗
PubMed2006

Skin manifestations with Rotavirus infections.

Rotavirus infection is one the most frequent cause of diarrhea among infants and children. Although it is not associated to specific dermatologic clinical pictures, recently, different clinical manifestations have been reported in association with this infection. They include exanthema, Gianotti-Crosti syndrome, and Acute Infantile Hemorrhagic Edema. The condition can be diagnosed microbiologically with stool cultures. The prognosis is excellent in healthy, immunocompetent individuals.

Diarrhea↗
PubMed1993

Proteolytic enhancement of human rotavirus infectivity.

Rotaviruses are the most important etiologic agents of severe diarrhea worldwide. Despite great advances in vaccine development, little is known about host protection mechanisms other than immunity. This presentation focuses on the proteolytic enhancement of rotavirus infection, with emphasis on the functions of VP4, an outer capsid protein. The in vitro growth of human rotavirus is enhanced by trypsin, which selectively cleaves VP4. Treatment with trypsin increases the infectivity of human rotavirus while decreasing its hemagglutination activity. There are two modes of rotavirus internalization: direct penetration with the aid of trypsin and endocytosis without trypsin. Direct penetration via VP4 cleaved by trypsin is essential for the replication of the virus, whereas endocytotic internalization does not give rise to viral replication.

Animals↗
PubMedDate not supplied

[The status and outlook of the laboratory diagnosis of rotavirus infection].

Rotavirus infection is not only the most distributed disease of children but a widely spread cause of their death. Nowadays considerable methodical potential which permits effectively detecting the whole virions, group A, antigens of human rotaviruses, virus-specific RNA in the clinical material is accumulated. There is a tendency to an increase of sensitivity and expressivity of the methods based on the use of immunological principles for detection and calculation of the antigen-antibody complex. Molecular-biological methods of the study are developed, which is important for the theory and practice of this infection control.

Antibodies, Viral↗
PubMed2006

Clinical and epidemiological aspects of rotavirus infection.

Rotavirus is a major worldwide cause of infant morbidity and mortality, and disease burden in the US is substantial. Vaccination is the only practical way to gain control over rotavirus disease. Prevention through the universal use of improved live oral vaccines is on the horizon.

Acute Disease↗
PubMedDate not supplied

Neonatal rotavirus infections.

Rotavirus (RV) infections in newborns differ from those in older infants; the majority of RV infections that occur in neonates are mild or asymptomatic. Generally, fewer than one-third of RV-infected neonates have diarrhea, although rates have reached 77% in some hospital nursery populations. Cases with severe diarrhea, necrotizing enterocolitis, bowel perforation, and death have been reported, but such cases are very rare. Infection usually occurs during the first week of life and generally invokes a mucosal antibody response without a concomitant serologic antibody response. Neonatal RV infections appear to incite an immune response that affords significant protection against severe RV-associated diarrhea, although not necessarily against a symptomatic RV infection later in life. Strains that cause neonatal infections differ from those that infect older infants; the outer-capsid protein VP4 is highly conserved in "nursery" RV strains, a property that probably plays a key role in their attenuated virulence. Immaturity of proteolytic enzymes in the neonatal gut and presence of secretory anti-RV IgA and trypsin inhibitors in breast milk are other factors that could account for the asymptomatic nature of RV infections in newborns. Natural "nursery" strains of RV are currently being evaluated as vaccine candidates.

Antibodies, Viral↗
PubMed2006

Role of sialic acids in rotavirus infection.

Rotaviruses are the leading cause of childhood diarrhea. The entry of rotaviruses into the host cell is a complex process that includes several interactions of the outer layer proteins of the virus with different cell surface molecules. The fact that neuraminidase treatment of the cells, or preincubation of the virus with sialic acid-containing compounds decrease the infectivity of some rotavirus strains, suggested that these viruses interact with sialic acid on the cell surface. The infectivity of some other rotavirus strains is not affected by neuraminidase treatment of the cells, and therefore they are considered neuraminidase-resistant. However, the current evidence suggests that even these neuraminidase-resistant strains might interact with sialic acids located in context different from that of the sialic acids used by the neuraminidase-sensitive strains. This review summarizes our current knowledge of the rotavirus-sialic acid interaction, its structural basis, the specificity with which distinct rotavirus isolates interact with sialic acid-containing compounds, and also the potential use of these compounds as therapeutic agents.

Amino Acid Sequence↗
PubMed1989

Lack of impact of rapid identification of rotavirus-infected patients on nosocomial rotavirus infections.

The efficacy of rapid identification of rotavirus-infected patients in the control of nosocomial rotavirus infections on an infant and young toddler ward by use of a rotavirus antigen detection test on stool from patients with diarrhea was evaluated by comparing the rate of nosocomial rotavirus infection in children during two separate 5-week periods in the winters of 1984 and 1986. In contrast to 1984 rapid rotavirus antigen testing by latex agglutination of stool from patients with diarrhea was instituted in 1986, in addition to testing for rotavirus by enzyme immunoassay, to determine whether use of rapid antigen testing resulted in an increased incidence of appropriate isolation and a decrease in nosocomial infections. In 1986 rapid identification of rotavirus resulted in an increase in hospitalization of rotavirus-infected patients in single bed rooms from 68% to 100% (P = 0.02, chi square test) but no significant increase in the use of enteric precautions for these patients. The total number of cases of nosocomial rotavirus infection in the two periods did not differ. In both periods 11 cases occurred; the nosocomial infection rate in 1984 was 18.9 cases/1000 days of exposure whereas in 1986 it was 20.2 cases/1000 days. These findings indicate that the use of rapid rotavirus antigen testing of patients with diarrhea is not of appreciable benefit in preventing the nosocomial spread of rotavirus to infants on the ward.

Cross Infection↗