Viral Diseases of the Digestive System

Kraft, Lisbeth M.

doi:10.1016/b978-0-12-262502-2.50016-x

Cited by 13 publications

(13 citation statements)

References 252 publications

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“…virus titer in intestinal tissue sample taken 1 HP1 never exceeded the ated virus dose which indicates that these isolates were undergoing the phases of replication cycle. This observation is consistent with prevj ious reports (Eydelloth et al, 1984;Gouvea et al, 1986;Kraft, 1982;Offrt et al, 191 64;Ramig, 1988;Starkey et al, 1986;Wolf et al, 1981). However, the peaks of infectious virus occurred earlier than in other studies, suggesting that the rate of replication of both the isolates is much faster than other human and animal ro 'tavirus isolates used in mouse models.…”

Section: Discussionsupporting

confidence: 89%

“…The MRV was much more virulent than other human or animal rotaviruses used in this model. Clinical symptoms observed using BRV or MRV in the present study were found to be in accord with EDIM as reported elsewhere (Kraft, 1982) with the only difference being that they occurred much earlier in this study than what has been reported for EDIM and other rotavirus isolates using a mouse model (Kraft, 1982;Offit et al, 1984).…”

Section: Discussionsupporting

confidence: 87%

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Development of a murine model to study the pathogenesis of rotavirus infection

Ijaz

Dent

Haines

et al. 1989

Experimental and Molecular Pathology

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A murine model to study enteritis induced by bovine (BRV) and murine rotavirus (MRV) has been developed. The course of infection was determined by clinical symptoms of diarrhea and virus isolation as well as histopathological, immunohistochemical, and electron microscopic methods. Both isolates were able to replicate and produce clinical symptoms in neonatal mice. Rotavirus-free neonates were orally inoculated with MRV or BRV and observed over a 192-hr postinoculation (HPI) period. Following infection with 10(4) PFU of virus, diarrhea and maximal intestinal dysfunction, as measured by xylose absorption, did not occur until beyond 20 hr postinfection even though maximal virus production occurred at 10-15 HPI. Immunohistochemically and by electron microscopy we were able to demonstrate viral antigen and virus particles in the enterocytes of villous tips at 5-8 HPI. The appearance of diarrheal symptoms was dependent on the virus dose and the type of virus isolate inoculated. The disease could be induced with doses as low as 1 x 10(2) PFU/mouse of BRV and 1 x 10(1) PFU/mouse of MRV. On the basis of these results, MRV was found to be more virulent than BRV in this model. The model should prove useful for studies designed to assess rotavirus virulence genes and for vaccine protection studies. This work emphasizes the need for early sample collection for critical evaluation of any vaccine or antiviral agent using this model.

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Section: Discussionsupporting

confidence: 89%

Section: Discussionsupporting

confidence: 87%

Development of a murine model to study the pathogenesis of rotavirus infection

Ijaz

Dent

Haines

et al. 1989

Experimental and Molecular Pathology

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“…M. Kraft performed some of the early studies of rotavirus infection, using epidemic diarrhea of infant mice virus (EDIM) before it was recognized as a rotavirus (1). An important but under-appreciated aspect of this work is that rotavirus spread throughout the bodies of the infected mice following oral infection (39,40,41). By 72 h postinfection, infectious EDIM was found in the lungs, liver, spleen, kidney, bladder, brain, and blood.…”

Section: Systemic Infection With Rotavirusmentioning

confidence: 99%

Pathogenesis of Intestinal and Systemic Rotavirus Infection

Ramig

2004

J Virol

316

230

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Rotaviruses are responsible for significant gastrointestinal disease, primarily in children Ͻ5 years of age and the young of other mammalian species. Each year rotaviruses cause approximately 111 million episodes of gastroenteritis in children, which result in 25 million visits to clinics, 2 million hospitalizations, and 352,000 to 592,000 deaths. On a worldwide basis, nearly every child experiences rotavirus gastroenteritis by age 5, 1 in 5 visits a clinic, 1 in 65 is hospitalized, and 1 in 293 dies. Children in the poorest countries account for 82% of rotavirus deaths (60). This disease burden underscores a need for interventions such as vaccines. A vaccine was developed and approved, but recommendation for its use was withdrawn because of vaccination-associated adverse events (57). Additional information about the molecular biology, immunology, and pathogenesis of rotavirus infection will inform ongoing vaccine development efforts.Our understanding of rotavirus-induced diarrheal disease is incomplete compared to that of several other pathogens (e.g., cholera). Rotavirus diarrhea has been attributed to several different mechanisms, including malabsorption secondary to enterocyte destruction, a virus-encoded toxin, stimulation of the enteric nervous system (ENS), and villus ischemia (13,45). Over the past several years, numerous studies have addressed mechanisms of diarrhea induction at the cellular and tissue levels, and a new understanding of the mechanisms is beginning to emerge. Here I will briefly outline the new data and present our current understanding of how rotaviruses induce diarrhea in the infected host.Recent studies confirm sporadic case reports that rotavirus infection is not confined to the intestine as was generally assumed. Although systemic sequellae to rotavirus infection are apparently rare, reports have continually appeared in the literature, and recent work with animal models has begun to shed light on how the virus spreads to extraintestinal sites. Our current understanding of extraintestinal spread and infection will also be considered below. GENERAL CHARACTERISTICS OF ROTAVIRUS INFECTION AND DISEASE IN HUMANS AND ANIMALSRotavirus. Rotaviruses comprise a genus within the family Reoviridae. The rotavirion has a nonenveloped, complex, triple-layered capsid structure that surrounds a genome composed of 11 segments of double-stranded RNA. There are six structural proteins and six nonstructural proteins, each encoded in a unique genome segment except for nonstructural proteins 5 and 6 (NSP5 and NSP6), which are encoded in overlapping reading frames of a single segment. The rotavirus genus is divided into serological groups (A to E). Groups A to C infect humans, and all groups infect animals. All the information presented here is in regard to group A virus infections.Pathophysiology of rotavirus diarrhea. The enterocytes lining the small intestine are generally divided into two types: enterocytes and crypt cells (Fig. 1). Villus enterocytes are mature, nonproliferating cells covering the vill...

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“…The absence of autoimmune disease in our model remains to be explained. In fact, mice infected with MHV-A59 develop acute hepatitis but liver regeneration may take place as early as 10e14 days after infection [6,8]. Additionally, other MHV-A59 effects, such as thymus involution, the enlargement of the spleen and production of great amounts of IgG2a, are also transient [9,10,21].…”

Section: Discussionmentioning

confidence: 99%

Sequence similarity and structural homologies are involved in the autoimmune response elicited by mouse hepatitis virus A59

Mathieu

Gómez

Coutelier

et al. 2004

Journal of Autoimmunity

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The features of autoantibodies (autoAb) to liver fumarylacetoacetate hydrolase (FAH) elicited in mice infected with mouse hepatitis virus (MHV) were studied by ELISA and western-blot competition assays. All sera tested contained Ab to cryptic FAH epitopes according with results from western-blot tests, whereas ELISA data indicated that some of these same sera did recognize native epitopes of the autoantigen (autoAg). Such differences were detected in individual sera from various mouse strains, and were ascribed to the fact that proteins insolubilized on solid supports expose a variety of conformational and cryptic antigenic determinants. On the other hand, whereas results from both experimental protocols showed that anti-MHV Ab did not cross-react with the soluble autoAg, the opposite situation did not show analogous results. Thus, binding of autoAb to insolubilized FAH could be inhibited by MHV depending on the mouse serum or the experimental protocol used. Additionally, a set of synthetic homologous peptides from mouse FAH and various viral proteins was employed to analyze the Ab repertoire of MHV-infected mice. Results indicated that two homologous peptides were recognized by most Ab: the N-terminal sequences (1-10) from FAH and the nucleocapside, both sharing 50% of identity, and sequence 2317-2326 of the RNA polymerase, a peptide showing 30% of identity with FAH 11-20. Results indicated that MHV-infection triggers at least three distinct Ab populations: anti-MHV, anti-FAH and cross-reacting Ab. This cross-reaction implies either sequential or conformational epitopes from both the viral proteins and the autoAg and may differ between individuals.

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Viral Diseases of the Digestive System

Cited by 13 publications

References 252 publications

Development of a murine model to study the pathogenesis of rotavirus infection

Development of a murine model to study the pathogenesis of rotavirus infection

Pathogenesis of Intestinal and Systemic Rotavirus Infection

Sequence similarity and structural homologies are involved in the autoimmune response elicited by mouse hepatitis virus A59

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