The pathogenicity of two porcine rotaviruses differing in their in vitro growth characteristics and genes 4

Bridger, Janice C.; Burke, Bernard; Beards, G. M.; Desselberger, Ulrich

doi:10.1099/0022-1317-73-11-3011

Cited by 26 publications

(24 citation statements)

References 24 publications

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“…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). The similar severities of diarrhea in PRV G9P [13]-and HRV Wa G1P [8]-inoculated pigs indicated that these two RVA strains might have similar rates of replication in mature enterocytes of the small intestine, causing similar damage to the gut epithelium.…”

Section: Discussionmentioning

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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Section: Discussionmentioning

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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“…In addition, it was not clear whether the major prevalent G2 rotavirus found in the 1993 epidemic had became more virulent. Further studies of the virulenceassociated VP4 and NSP4 genes (Offit et al, 1986 ;Bridger et al, 1992 ;Hoshino et al, 1995 ;Ball et al, 1996) would be required.…”

Section: Discussionmentioning

confidence: 99%

Sequence analysis of VP1 and VP7 genes suggests occurrence of a reassortant of G2 rotavirus responsible for an epidemic of gastroenteritis.

Zao

Kao

et al. 1999

Journal of General Virology

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G2 rotavirus was prevalent in a 1993 epidemic of acute gastroenteritis in Taiwan. In this study, the genetic relationship among G2 rotavirus strains was analysed. The VP7 genes were amplified and sequenced. Except for one strain isolated in 1981, the nucleotide sequences of the VP7 genes of most of the G2 rotaviruses were very similar (identity 97 %) and were closely related to that of a Japanese G2 reference strain, S2. The genetic relatedness of G2 rotaviruses was analysed further by RNA-RNA hybridization. The genomes of the major G2 strains of 1993 did not hybridize well with those of the G2 strains of previous seasons in RNA segments 1, 6 and 7. Partial nucleotide sequences of the VP1 gene were analysed and appeared to be similar among the major G2 strains from the same epidemic (identity 98 %), whereas the identity of the VP1 genes of the major G2 strains of the 1993 epidemic to those of previous seasons was only about 84 %. Since the numbers of mutations accumulated in the VP1 and VP7 genes over a period of 10 years were comparable, the significant change in the VP1 genes of the major strains of the 1993 epidemic suggests that these G2 rotaviruses had evolved by genetic reassortment.

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“…Recently, analyses of VP7 and VP4 nucleotide and deduced amino acid sequences of Mc323 and Mc345 revealed that both strains belonged to G9P [19] genotype (41), with the VP7 sequences closely related to the G9 human rotaviruses WI61 and F45, while the VP4 sequence revealed a close genetic relatedness to that of the P [19] porcine rotavirus 4F reported previously (2). Most recently, a human rotavirus G9P [19] isolate (RMC321) with porcine rotavirus characteristics was also reported following an outbreak of infantile gastroenteritis in India (55).…”

mentioning

confidence: 99%

Detection of Rare G3P[19] Porcine Rotavirus Strains in Chiang Mai, Thailand, Provides Evidence for Origin of the VP4 Genes of Mc323 and Mc345 Human Rotaviruses

Maneekarn¹,

Khamrin

Chan-it³

et al. 2006

J Clin Microbiol

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The pathogenicity of two porcine rotaviruses differing in their in vitro growth characteristics and genes 4

Cited by 26 publications

References 24 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]

Sequence analysis of VP1 and VP7 genes suggests occurrence of a reassortant of G2 rotavirus responsible for an epidemic of gastroenteritis.

Detection of Rare G3P[19] Porcine Rotavirus Strains in Chiang Mai, Thailand, Provides Evidence for Origin of the VP4 Genes of Mc323 and Mc345 Human Rotaviruses

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