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Nosocomial rotavirus infection in European countries: a review of the epidemiology, severity and economic burden of hospital-acquired rotavirus disease.

The data currently available on the epidemiology, severity and economic burden of nosocomial rotavirus (RV) infections in children younger than 5 years of age in the major European countries are reviewed. In most studies, RV was found to be the major etiologic agent of pediatric nosocomial diarrhea (31-87%), although the number of diarrhea cases associated with other virus infections (eg, noroviruses, astroviruses, adenoviruses) is increasing quickly and almost equals that caused by RVs. Nosocomial RV (NRV) infections are mainly associated with infants 0-5 months of age, whereas community-acquired RV disease is more prevalent in children 6-23 months of age. NRV infections are seasonal in most countries, occurring in winter; this coincides with the winter seasonal peak of other childhood virus infections (eg, respiratory syncytial virus and influenza viruses), thus placing a heavy burden on health infrastructures. A significant proportion (20-40%) of infections are asymptomatic, which contributes to the spread of the virus and might reduce the efficiency of prevention measures given as they are implemented too late. The absence of effective surveillance and of reporting of NRV infections in any of the 6 countries studied (France, Germany, Italy, Poland, Spain and the United Kingdom) results in severe underreporting of NRV cases in hospital databases and therefore in limited awareness of the importance of NRV disease at country level. The burden reported in the medical literature is potentially significant and includes temporary reduction in the quality of children's lives, increased costs associated with the additional consumption of medical resources (increased length of hospital stay) and constraints on parents'/hospital staff's professional lives. The limited robustness and comparability of studies, together with an evolving baseline caused by national changes in health care systems, do not presently allow a complete and accurate overview of NRV disease at country level to be obtained. RV is highly contagious, and the efficiency of existing prevention measures (such as handwashing, isolation and cohorting) is variable, but low at the global level because of the existence of numerous barriers to implementation (eg, lack of staff, high staff turnover, inadequate hospital infrastructure). Prevention of RV infection by mass vaccination could have a positive impact on the incidence of NRV by reducing the number of children hospitalized for gastroenteritis, therefore reducing the number of hospital cross-infections and associated costs.

Child, Preschool↗

Rotavirus 993/83, isolated from calf faeces, closely resembles an avian rotavirus.

Polypeptides from purified virions of the calf rotavirus (RV) isolate 993/83 and those from the pigeon RV isolate PO-13 comigrated on SDS-polyacrylamide gels. Two polypeptides of 45K and 47K were detected at the position of VP6. Both proteins behaved like authentic VP6 protein with EDTA and heat treatment. RV 993/83 and PO-13 showed identical one-dimensional peptide maps for VP2, and the 45K and 47K proteins. More than 70% of sera from German cattle older than 1 year showed neutralizing serum antibodies to RV 993/83 and RV PO-13.

Animals↗

Molecular biology of rotaviruses. III. Isolation and characterization of temperature-sensitive mutants of bovine rotavirus.

Twenty-six temperature-sensitive (ts) mutants of United Kingdom tissue culture-adapted bovine rotavirus were isolated and characterized. Fourteen of these mutants were determined to be ts both by efficiency of plating and by virus yield at the nonpermissive temperature of 39.5 degrees C as compared with that at the permissive temperature of 32 degrees C. The remaining mutants were only ts by the criterion of efficiency of plating. High-frequency recombination (gene reassortment) was observed when some pairs of mutants were crossed, and this allowed the classification of the mutants into five separate recombination groups. Groups III and V have prototype ts mutants (ts34 and ts115, respectively) that do not synthesize RNA or polypeptides at 39.5 degrees C. The other groups, I, II, and IV, have prototype mutants (ts17, ts7, and ts6, respectively) that synthesize both RNA and polypeptides at 39.5 degrees C, although ts17 does so only at a reduced level.

Cytopathogenic Effect, Viral↗

Molecular biology of rotaviruses. IV. Molecular cloning of the bovine rotavirus genome.

A new cloning strategy has been developed for cloning the genomes of double-stranded RNA viruses by using bovine rotavirus as a test system. The major modification adopted was the use of denatured polyadenylated double-stranded RNA as the template for reverse transcriptase. This allowed the two complementary strands of cDNA to be synthesized in a single reaction and removed the need for S1 nuclease digestion to remove the 5' hairpin structure normally generated in cDNA synthesis.

Animals↗

Nucleotide sequence of the gene encoding the serotype-specific antigen of human (Wa) rotavirus: comparison with the homologous genes from simian SA11 and UK bovine rotaviruses.

The nucleotide sequence of human (Wa) rotavirus genome segment 9, which encodes the serotype-specific antigen VP7, has been determined. Comparison of the deduced amino acid sequence of Wa VP7 protein to the sequences of simian SA11 and UK bovine VP7 proteins shows that the majority of the amino acid differences are clustered between amino acid residues 37 through 49, 65 through 75, 87 through 105, 122 through 126, 146 through 149, 178 through 181, and 208 through 242. A hydrophilicity profile of the three proteins reveals correlations between hydrophilic peaks, potentially antigenic determinants, and certain clusters of amino acid changes.

Amino Acid Sequence↗

Viral determinants of rotavirus pathogenicity in pigs: evidence that the fourth gene of a porcine rotavirus confers diarrhea in the homologous host.

A porcine rotavirus (prv) monoreassortant, S-F4, which carries RNA segment 4 of the pig-pathogenic variant prv 4F in the genetic background of the pig-apathogenic variant prv 4S (G. I. Tauscher and U. Desselberger, J. Virol. 71:853-857, 1997), was found to be pathogenic in gnotobiotic piglets. This indicates that RNA segment 4 of the pig-pathogenic variant prv 4F is a major determinant of pathogenicity in its homologous host.

Animals↗

Distribution of rotavirus antigen in intestinal lymphoid tissues: potential role in development of the mucosal immune response to rotavirus.

Groups of suckling BALB/c mice were inoculated with murine rotavirus (MRV) at 5 days of age and sequentially tested for the presence of MRV antigen (Ag) in intestinal villus epithelium (VE), Peyer's patch (PP), mesenteric lymph node (MLN), spleen, liver and lung, using indirect immunofluorescence techniques (IF). MRV Ag was first detected in VE 24 h after oral administration of the virus and remained in VE for as long as 10 days post-inoculation (pi). MRV Ag was observed in the epithelium overlying PP at 3-7 days pi and in subepithelial and interfollicular areas in the PP between 3 and 20 days pi. MRV Ag was also detected in MLN during the same period of time. Small numbers of MRV-Ag-containing cells were detected in the lamina propria (LP) of intestinal villi at 10 days pi. Most MRV-Ag-containing cells in PP and MLN were Ia-positive but negative for Lyt-1, Lyt-2 and MAC-1 cell surface markers. MRV-Ag-containing cells were negative for surface or cytoplasmic immunoglobulin. Intestinal antibody response to MRV indicated by the presence of MRV-specific IgA plasma cells in LP was first detectable 10 days pi. Highest density of MRV-specific plasma cells was observed in the duodenum, with a similar distribution to that of MRV-Ag-containing cells in PP. These observations suggest that MRV-Ag uptake is largely limited to the PP associated epithelium and the virus Ag is subsequently transported to the underlying lymphoid follicles and MLN. These findings suggest a close relationship between the availability of MRV Ag in the lymphoid follicles at different locations and the subsequent development of local antibody responses in different segments of small intestine.

Animals↗