Serial Studies of Virus Multiplication and Intestinal Damage in Gnotobiotic Piglets Infected with Rotavirus

Crouch, Colin; Woode, G. N.

doi:10.1099/00222615-11-3-325

Cited by 49 publications

(43 citation statements)

References 23 publications

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“…The increased cellularity of the lamina propria may also be one of the reasons for the paleness of the intestinal tract. The patterns of virus replication and antibody development in turkeys were similar to those seen in rotavirus-infected chicks (McNulty et al, 1983), and also with the infection cycle seen in mammalian species (Johnson et al, 1983a;Crouch and Woode, 1978;Mebus et al, 1971;TorresMedina et al, 1976b). The onset and duration of virus replication and the rapid increase of virus excretion were all typical for the pathogenesis of rotavirus infection.…”

Section: Discussionsupporting

confidence: 63%

“…Experimental infections have been reported in gnotobiotic piglets (Theil et al, 1978;McAdaragh et al, 1980;Pearson and McNulty, 1977;Crouch and Woode, 1978;Torres-Medina et al, 1976a and b), gnotobiotic calves (Mebus et al, 1971(Mebus et al, , 1977, lambs (Snodgrass et al, 1977), gnotobiotic dogs (Johnson et al, 1983a and b) and conventional suckling mice (Adams and Kraft, 1967), where the virus caused enteritis, diarrhoea and malabsorption. Experimental infection in chickens, reported by McNulty et al (1983) and Meulemans et al (1985), resulted in a mild or subclinical infection.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Pathogenesis of rotavirus infection in turkey poults

Yason

Schat

1986

Avian Pathology

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Section: Discussionsupporting

confidence: 63%

Section: Introductionmentioning

confidence: 99%

Pathogenesis of rotavirus infection in turkey poults

Yason

Schat

1986

Avian Pathology

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“…Fecal virus shedding peaked at PID 2 (2.56Eϩ06 FFU/ml) and then again at PID 5 in the HRV Wa G1P [8]-inoculated pigs (as observed in previous studies [51,52]), decreasing overall in the following days (PIDs 3 to 10), whereas fecal virus shedding of the PRV G9P [13]-inoculated pigs peaked at PID 3 (6.73Eϩ05 FFU/ ml), which was then maintained at higher and relatively constant levels (1.02Eϩ05 to 1.14Eϩ06 FFU/ml) through PID 10 (Fig. 1A).…”

Section: Prv G9pmentioning

confidence: 67%

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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“…It has been observed in rotavirus infections of lambs and pigs that the immunofluorescence of villi is maximal before villous atrophy develops (Snodgrass, Angus and Gray, 1977;Crouch and Woode, 1978).…”

Section: Pathologymentioning

confidence: 99%