Gastroenteritis Caused By Human Rotaviruses (Serotype Three) In A Suckling Mouse Model

Lm, Bell; Hf, Clark; Ea, O'Brien; Mj, Kornstein; Sa, Plotkin; Pa, Offit

doi:10.3181/00379727-184-rc2

Cited by 34 publications

(21 citation statements)

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“…2). This result confirmed that of Bell et al (3), in which serotype 3 human rotaviruses were able to cause gastroenteritis in suckling CD-1 mice. Human serotype 3 strain of rotavirus appears to be serotypically similar to at least one strain (EB) of murine rotavirus, as shown by Greenberg et al (14).…”

Section: Discussionsupporting

confidence: 82%

Gastroenteritis in Suckling Mice Caused by Human Rotavirus Can Be Prevented with Egg Yolk Immunoglobulin (IgY) and Treated with a Protein‐Bound Polysaccharide Preparation (PSK)

Ebina

Tsukada

Umezu

et al. 1990

Microbiology and Immunology

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Oral inoculation of human rotavirus MO strain (serotype 3) into 5-dayold BALB/c mice cause gastroenteritis characterized by diarrhea. Clinical symptoms, histopathological changes in the small intestine, and the detection of rotavirus antigen in enterocytes were all characteristic of rotavirus-induced gastroenteritis. Using this small animal model, passive protection of suckling mice against human rotavirus infection was achieved with the use of immunoglobulin (IgY) from the yolks of eggs of rotavirus-immunized hens. When IgY against a rotavirus strain homotypic to the challenge virus (MO strain) was administered in the mice, complete protection against rotavirus infection was achieved. On the other hand, with oral administration of IgY against a heterotypic strain (serotype 1 , Wa strain), a lower protective effect was nevertheless obtained. The four different strains of human rotavirus (Wa, KUN, MO, and ST3) were inactivated in vitro by treatment with PSK, a protein-bound polysaccharide preparation, in a dose-dependent manner . Oral administration of 2.5 mg of PSK caused a therapeutic effect on experimentally MO-infected suckling mice. The antiviral effect of PSK was indicated by the reduction of the duration of diarrhea.

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Section: Discussionsupporting

confidence: 82%

Gastroenteritis in Suckling Mice Caused by Human Rotavirus Can Be Prevented with Egg Yolk Immunoglobulin (IgY) and Treated with a Protein‐Bound Polysaccharide Preparation (PSK)

Ebina

Tsukada

Umezu

et al. 1990

Microbiology and Immunology

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“…These differences have been attributed to the specific nature of the host response and not to the virus, since vacuolization is also a characteristic feature of heterologous infections in mice (2,19,38). Mice usually do not develop any symptoms beyond 2 weeks of age, and infection of adult mice occurs without disease or histopathological lesions (7,18,43,46,61,67).…”

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confidence: 99%

Changes in Small Intestinal Homeostasis, Morphology,and Gene Expression during Rotavirus Infection of InfantMice

Boshuizen

Reimerink

Male

et al. 2003

J Virol

134

123

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Rotavirus is the most important cause of infantile gastroenteritis. Since in vivo mucosal responses to a rotavirus infection thus far have not been extensively studied, we related viral replication in the murine small intestine to alterations in mucosal structure, epithelial cell homeostasis, cellular kinetics, and differentiation. Seven-day-old suckling BALB/c mice were inoculated with 2 ؋ 10 4 focus-forming units of murine rotavirus and were compared to mock-infected controls. Diarrheal illness and viral shedding were recorded, and small intestinal tissue was evaluated for rotavirus (NSP4 and structural proteins)-and enterocyte-specific (lactase, SGLT1, and L-FABP) mRNA and protein expression. Morphology, apoptosis, proliferation, and migration were evaluated (immuno)histochemically. Diarrhea was observed from days 1 to 5 postinfection, and viral shedding was observed from days 1 to 10. Two peaks of rotavirus replication were observed at 1 and 4 days postinfection. Histological changes were characterized by the accumulation of vacuolated enterocytes. Strikingly, the number of vacuolated cells exceeded the number of cells in which viral replication was detectable. Apoptosis and proliferation were increased from days 1 to 7, resulting in villous atrophy. Epithelial cell turnover was significantly higher (<4 days) than that observed in controls (7 days). Since epithelial renewal occurred within 4 days, the second peak of viral replication was most likely caused by infection of newly synthesized cells. Expression of enterocyte-specific genes was downregulated in infected cells at mRNA and protein levels starting as early as 6 h after infection. In conclusion, we show for the first time that rotavirus infection induces apoptosis in vivo, an increase in epithelial cell turnover, and a shutoff of gene expression in enterocytes showing viral replication. The shutoff of enterocyte-specific gene expression, together with the loss of mature enterocytes through apoptosis and the replacement of these cells by less differentiated dividing cells, likely leads to a defective absorptive function of the intestinal epithelium, which contributes to rotavirus pathogenesis.Rotaviruses are one of the most significant causes of gastroenteritis, malnutrition, and diarrhea in young children and animals (17, 28). Mortality rates are low in developed countries, where illness is usually self-limiting (64). However, each year more than 600,000 young children die in developing countries throughout the world (26). Rotavirus infection in children is mainly restricted to the small intestinal villus epithelium, resulting in the occurrence of total villus atrophy (3). Although rotavirus can infect older children and adults, diarrheal disease is primarily observed in children under 2 years of age (16,17,28).Rotavirus-induced diarrhea is thought to be caused by a combination of factors (55), which include a reduction in epithelial surface area, replacement of mature enterocytes by immature (crypt-like) cells (43), an osmotic effect resulting from ...

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“…RRV may be more stable than RRV-human reassortant viruses [10]. Alternatively, heterologous host G3 strains have been shown to replicate in mice better than non-G3 strains [11]; RRV is similar to human G3 rotavirus strains. RRV also has been shown to replicate in rabbits with greater efficiency than other heterologous host rotaviruses [12].…”

Section: Discussionmentioning

confidence: 98%

Hypertrophy, Hyperplasia, and Infectious Virus in Gut‐Associated Lymphoid Tissue of Mice after Oral Inoculation with Simian‐Human or Bovine‐Human Reassortant Rotaviruses

Moser¹,

Dolfi²,

Vietro³

et al. 2001

J INFECT DIS

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Oral inoculation of infants with a vaccine that contains simian-human reassortant rotaviruses has been found to be a rare cause of intussusception. Because intussusception can be associated with enlargement of gut-associated lymphoid tissue, we studied the capacity of simian-human and bovine-human reassortant rotaviruses to cause lymphoid hypertrophy and hyperplasia of Peyer's patches (PP) of adult BALB/c mice. Neither hypertrophy nor hyperplasia was detected in PP after oral inoculation with simian-human or bovine-human reassortant rotaviruses. However, infectious virus was detected in PP and mesenteric lymph nodes after oral inoculation with simian, but not bovine, reassortant rotaviruses. Implications of these findings on the pathogenesis of intussusception are discussed.A vaccine that contains simian-human reassortant rotaviruses was found to be a rare cause of intussusception in infants [1]. The vaccine (Rotashield; Wyeth-Lederle Laboratories) contained simian rotavirus strain RRV and 3 simian-human reassortant rotaviruses. In contrast, natural infection with rotavirus is not clearly a cause of intussusception [2].Although why the simian-based rotavirus vaccine caused intussusception remains unclear, several hypotheses have been advanced. First, lymphoid enlargement in gut-associated lymphoid tissue (GALT) caused by simian rotaviruses may serve as a "lead point" for intussusception. Second, the vaccine strain may replicate in a site different from that of natural infection. Finally, the vaccine strain(s) may be processed or presented by antigen-presenting cells in a site or manner different from that which occurs after natural infection.We examined the capacity of the simian-based reassortant rotavirus vaccine to cause lymphoid hypertrophy or hyperplasia of Peyer's patches (PP) after oral inoculation of adult BALB/ c mice. In addition, we determined whether infectious rotavirus could be detected in GALT. These findings were compared with those for mice orally inoculated with either a bovine-based reassortant rotavirus vaccine or media alone.

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Gastroenteritis Caused By Human Rotaviruses (Serotype Three) In A Suckling Mouse Model

Cited by 34 publications

References 0 publications

Gastroenteritis in Suckling Mice Caused by Human Rotavirus Can Be Prevented with Egg Yolk Immunoglobulin (IgY) and Treated with a Protein‐Bound Polysaccharide Preparation (PSK)

Gastroenteritis in Suckling Mice Caused by Human Rotavirus Can Be Prevented with Egg Yolk Immunoglobulin (IgY) and Treated with a Protein‐Bound Polysaccharide Preparation (PSK)

Changes in Small Intestinal Homeostasis, Morphology,and Gene Expression during Rotavirus Infection of InfantMice

Hypertrophy, Hyperplasia, and Infectious Virus in Gut‐Associated Lymphoid Tissue of Mice after Oral Inoculation with Simian‐Human or Bovine‐Human Reassortant Rotaviruses

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