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1.  Epidemiology of group C rotavirus infection in Western New York women of childbearing age. 
Journal of Clinical Microbiology  1997;35(2):486-488.
Umbilical cord serum samples (380), an average of 10 per month for 3 years (1990 to 1992), were tested by indirect immunofluorescence assay for group C rotavirus immunoglobulin G. Thirty percent were positive, suggesting that approximately one-third of women of childbearing age in western New York have experienced group C rotavirus infection.
PMCID: PMC229607  PMID: 9003623
2.  VP4 genotyping of human rotavirus in the United States. 
Journal of Clinical Microbiology  1994;32(1):205-208.
The VP4 (P) and VP7 (G) types of 171 rotavirus isolates obtained from children with diarrhea in the United States were characterized by PCR typing assays. Strains P1G1 predominated (71%); this was followed by strains P1G3 (20%) and P2G2 and P1G4 (2% each). Mixed types were identified in five (3%) specimens. Two (1%) strains bearing the P3 genotype (P3G1 and P3G2) were found in children with severe dehydrating diarrhea, although the P3 genotype has been regarded as a possible marker for virus attenuation.
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PMCID: PMC262997  PMID: 8126181
3.  Extramucosal spread and development of hepatitis in immunodeficient and normal mice infected with rhesus rotavirus. 
Journal of Virology  1990;64(1):361-368.
The pathogenic profiles of two heterologous animal rotaviruses, rhesus rotavirus strain MMU 18006 and bovine rotavirus strain WC3, were evaluated in mice with severe combined immunodeficiency (SCID mice) and normal BALB/c mice. Control animals were inoculated with homologous murine strain EDIM 5099 or a tissue culture-adapted murine rotavirus. Heterologous infection with rhesus rotavirus resulted in hepatitis in 84% of SCID and 21% of BALB/c mice, with mortality rates of 27 and 0%, respectively. Surviving SCID animals developed chronic liver disease, while symptoms in BALB/c mice resolved in 2 to 4 weeks after onset. Histopathologic examination revealed a diffuse hepatitis with focal areas of parenchymal necrosis. Rotavirus was detected in liver tissue from 100% of 29 SCID and 85% (11 of 13) BALB/c animals tested by cell culture infectivity, immunofluorescence, or electron microscopy. No extramucosal spread of virus or hepatitis was observed after infection with heterologous bovine strain WC3 or homologous murine rotaviruses. This finding of a novel rotavirus-induced disease manifestation suggests altered tissue tropism in a heterologous host for a group of viruses previously shown to replicate exclusively in the gut mucosa. The implications of our observations suggest that in human vaccine trials utilizing heterologous rotavirus strains, special attention should be paid to children with immunodeficiency disorders, and screening for hepatic function should be included in vaccine protocols.
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PMCID: PMC249110  PMID: 2152822
4.  Persistent rotavirus infection in mice with severe combined immunodeficiency. 
Journal of Virology  1987;61(10):3345-3348.
Rotaviruses are important pathogens of human infants and the infants of many animal species. The disease produced by these viruses can be described as an acute, self-limiting diarrheal disease, with virus replication localized to the differentiated epithelial enterocytes of the small intestine. Immunologically normal infants shed virus for approximately 5 to 12 days after the onset of infection. Recently, it has been shown that rotavirus can produce a chronic infection in severely immunocompromised children, with virus shedding and intermittent diarrhea lasting from 6 weeks to 2 years (G. A. Losonsky, J. P. Johnson, J. A. Winkelstein, and R. H. Yolken, J. Clin. Invest. 76:2362-2367, 1985; F. T. Saulsbury, J. A. Winkelstein, and R. H. Yolken, J. Pediatr. 97:61-65, 1980). These findings point to an important role for the immune system in recovery from the disease. The study described here examined the outcome of murine rotavirus infection in mice with severe combined B- and T-cell immunodeficiency (SCID) and in immunologically normal seronegative BALB/c mice. Persistent rotavirus infection was established in all mice with SCID which had been inoculated orally as pups. Low levels of virus replication and constant fecal virus shedding characterized the chronic infection. This is the first report of a persistent rotavirus infection in an animal model.
PMCID: PMC255923  PMID: 3041056
5.  Potential spectrum of etiological agents of viral enteritis in hospitalized infants. 
Journal of Clinical Microbiology  1983;17(2):352-356.
Fecal specimens were obtained from 1,160 infants and young children with acute nonbacterial gastroenteritis over a period of 2 years. A total of 100 specimens were obtained from age-matched asymptomatic controls. The specimens were examined for the presence of viruses by electron microscopy. Viruses or virus-like particles frequently associated with enteritis were detected in 27% (314 of 1,160) of the symptomatic patients. No viruses or virus-like particles were detected in the 100 control subjects. Rotavirus was detected in 73% (230 of 314) of the virus-positive samples. The mean age of rotavirus-positive patients was 11.5 months, although the patients ranged in age from 2 weeks to 5 years. Of the symptomatic patients, 45 (14%) exhibited small virus-like particles (15 to 40 nm) in the feces in the absence of any other detectable pathogen. Some of the virus-like particles observed in these patients appeared to be similar to astrovirus, and some appeared to be similar to the Otofuke agent or possibly minireovirus. Significantly, however, the mean age of infants with enteritis from whom these small virus-like particles were recovered was 4.5 months (range, 10 days to 19 months). Our findings confirmed the already-known fact that rotaviruses constitute the most important cause of viral enteritis in young children. In addition, small viruses may be an important cause of gastroenteritis in infants under 5 months of age.
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PMCID: PMC272636  PMID: 6403578

Results 1-5 (5)