Pathogenesis of rotavirus-induced diarrhea

Graham, David Y.; Sackman, Jeffrey W.; Estes, Mary K.

doi:10.1007/bf01311255

Cited by 70 publications

(19 citation statements)

References 42 publications

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“…Mature enterocytes of the small intestine are the main target for RVs, which infect and destroy them, causing diarrhea (66,67). Pathogenic RVs replicated faster in piglets and calves than did apathogenic RVs, with enterocyte losses from pathogenic RV infection surpassing their physiologic replacement (68)(69)(70).…”

Section: Discussionmentioning

confidence: 99%

Comparative In Vitro and In Vivo Studies of Porcine Rotavirus G9P[13] and Human Rotavirus Wa G1P[8]

Shao

Fischer

Kandasamy

et al. 2016

J Virol

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The changing epidemiology of group A rotavirus (RV) strains in humans and swine, including emerging G9 strains, poses new challenges to current vaccines. In this study, we comparatively assessed the pathogenesis of porcine RV (PRV) G9P IMPORTANCEThe changing epidemiology of porcine and human group A rotaviruses (RVs), including emerging G9 strains, may compromise the efficacy of current vaccines. An understanding of the pathogenesis and genetic, immunological, and biological features of the new emerging RV strains will contribute to the development of new surveillance and prevention tools. Additionally, studies of cross-protection between the newly identified emerging G9 porcine RV strains and a human G1 RV vaccine strain in a susceptible host (swine) will allow evaluation of G9 strains as potential novel vaccine candidates to be included in porcine or human vaccines. R otavirus (RV), a member of the Reoviridae family, has a double-stranded RNA genome with 11 segments (1). It is the most common pathogen in cases of acute gastroenteritis in children under 5 years of age (1, 2). In the United States, it causes approximately $1 billion in annual costs due to RV-associated physician visits, emergency department visits, and hospitalizations (3-5). Annually, RV causes 440,000 deaths in children under 5 years of age worldwide, with most occurring in developing countries (4). RVs also infect young domestic animals, including calves and piglets (1). RV is responsible for annual mortality rates of 7 to 20% and 3 to 15% in nursing and weaned piglets, respectively (6). The high prevalence of RV in swine results in large economic losses to the pork industry (6). Treatment of RV infection is possible only by replacing fluids and electrolyte losses, because no specific antiviral therapy is available. Therefore, effective RV vaccines are crucial to prevent morbidity and mortality in both young children and animals (7,8).RVs are classified into 8 groups, groups A to H, as determined by viral structural protein 6 (VP6) (9-11). Based on the outer capsid VP4 (P genotype)-and VP7 (G genotype)-encoding genes, a binary classification system has been established for RVs (12). Overall, there are at least 26 G genotypes and 33 P genotypes of group A RVs (RVAs) (13,14). Globally, the G1 to G4, P[4], P[6], and P [8] genotypes are the most prevalent human RVAs (15). RVA G1P[8] is a common human strain worldwide and constitutes Ͼ70% of prevalent strains in North America, Australia, and Europe but only 20 to 35% of circulating strains in South America, Asia, and Africa (5,(15)(16)(17). G5 and P[7] are historically considered the most prevalent G and P RVA genotypes in swine, respectively (18). However, recent studies have shown that RVA G9 and G12 genotypes are emerging worldwide in humans and swine (2,(19)(20)(21)(22)(23).

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Section: Discussionmentioning

confidence: 99%

Comparative In Vitro and In Vivo Studies of Porcine Rotavirus G9P[13] and Human Rotavirus Wa G1P[8]

Shao

Fischer

Kandasamy

et al. 2016

J Virol

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“…In spite of the fact that RV is the most common cause of diarrheal illness in young children, the knowledge of the molecular and cellular bases of host responsiveness to this infection remain scant. It is generally accepted that the destruction of villous epithelial cells reduces enzymatic and absorptive capacity in the small intestine (10), and the inflammatory response contributes to a secretory‐type diarhea (11). As TAC is significantly metabolized in the intestine, it can be assumed that the drug's metabolism will be influenced by conditions that alter intestinal function.…”

Section: Discussionmentioning

confidence: 99%

Rotavirus infection as cause of tacrolimus elevation in solid‐organ‐transplanted children

Frühwirth

Fischer

Simma

et al. 2001

Pediatric Transplantation

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Rotavirus (RV) is the most common cause of diarrheal illness in children. We report three solid-organ-transplanted patients in whom RV infection caused increased trough levels of the immunosuppressive macrolide tacrolimus (TAC) by mechanisms that are still under investigation. The virus was detected for longer in the feces of these patients than in infants not receiving immunosuppressive therapy. In association with short-term monitoring of blood trough levels of TAC, the dosage should be reduced early if symptoms of an acute gastroenteritis are present.

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“…Previous studies illustrate that short villi resulted in a reduction of villi surface area and digestive enzymes (Graham et al, 1984). Villus shortening occurs via an increase in rate of cell loss, leading to increased crypt cell production and, finally, increased crypt depth (Pluske et al, 1997).…”

Section: Intestine Morphologymentioning

confidence: 99%

Effects of Saccharomyces cerevisiae fermentation products on dairy calves: Ruminal fermentation, gastrointestinal morphology, and microbial community

Xiao

Alugongo

Chung

et al. 2016

Journal of Dairy Science

106

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The aim of this study was to evaluate the effects of Saccharomyces cerevisiae fermentation products (SCFP) in the calf starter and milk on ruminal fermentation, gastrointestinal morphology, and microbial community in the first 56 d of life. Thirty Holstein bull calves were randomly assigned to 1 of 3 groups: a texturized calf starter containing 0 (CON), 0.5, or 1% SCFP (XPC, Diamond V, Cedar Rapids, IA) of dry matter from d 4 to 56. In addition, the XPC-supplemented calves were fed with 1 g/d SCFP (SmartCare, Diamond V, Cedar Rapids, IA) in milk from d 2 to 30. All calves were fed 4 L of colostrum within 1 h of birth and were subsequently fed milk twice daily until weaned on d 56. Rumen fluid was collected by an esophageal tube 4 h after the morning feeding on d 28 and 56 to determine ruminal pH, ammonia-N, and volatile fatty acids concentrations. On d 56, 15 (5 per treatment) calves were harvested and slaughter weight, gastrointestinal morphology parameters, and bacteria community were recorded. Papilla length, width, and surface area were measured from 5 locations within the rumen. Villus height, width, surface area, crypt depth, and villus height-to-crypt depth ratio were measured in the duodenum, jejunum, and ileum. Next-generation sequencing technology was used to test the microbial community of the rumen and duodenum samples on d 28 and 56. Data were analyzed by MIXED procedure in SAS (SAS Institute Inc., Cary, NC) with contrast statements to declare CON versus all SCFP and 0.5 versus 1% SCFP in starter grains. Ruminal pH, ammonia-N, and total volatile fatty acids were not altered by SCFP. However, the supplemented groups exhibited higher ruminal butyrate concentrations coinciding with higher Butyrivibrio and lower Prevotella richness than CON group. Supplementation of SCFP increased papilla length in the rumen. In the small intestine, SCFP reduced crypt depth of jejunum, and increased villus height-to-crypt depth ratio in all segments of the small intestine, especially when supplemented at a higher dosage in the starter. In conclusion, Saccharomyces cerevisiae fermentation products improved gastrointestinal morphology, possibly due to increased Butyrivibrio and decreased Prevotella richness of the rumen fluid, which resulted in an increase in butyrate production, and the effect was slightly greater with the higher dosage of SCFP in the starter.

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Pathogenesis of rotavirus-induced diarrhea

Cited by 70 publications

References 42 publications

Comparative In Vitro and In Vivo Studies of Porcine Rotavirus G9P[13] and Human Rotavirus Wa G1P[8]

Comparative In Vitro and In Vivo Studies of Porcine Rotavirus G9P[13] and Human Rotavirus Wa G1P[8]

Rotavirus infection as cause of tacrolimus elevation in solid‐organ‐transplanted children

Effects of Saccharomyces cerevisiae fermentation products on dairy calves: Ruminal fermentation, gastrointestinal morphology, and microbial community

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