A Lymphatic Mechanism of Rotavirus Extraintestinal Spread in the Neonatal Mouse

Mossel, Eric C.; Ramig, Robert F.

doi:10.1128/jvi.77.22.12352-12356.2003

Cited by 63 publications

(63 citation statements)

References 25 publications

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“…Similarly, MLN in infected infants of diabetes-resistant mice harbour infectious RRV. The cells in the MLN involved are unidentified, although mouse rotavirus replicates in dendritic cells (DC), and possibly B cells and macrophages [21,22]. The spread of rotavirus to the MLN and PLN in adult mice has not been reported.…”

Section: Introductionmentioning

confidence: 99%

Rotavirus acceleration of murine type 1 diabetes is associated with a T helper 1-dependent specific serum antibody response and virus effects in regional lymph nodes

et al. 2012

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Aims/hypothesis Rotavirus infection in at-risk children correlates with production of serum autoantibodies indicative of type 1 diabetes progression. Oral infection with rhesus monkey rotavirus (RRV) accelerates diabetes onset in mice. This relates to their rotavirus-specific serum antibody titre and local pro-inflammatory cytokine induction without pancreatic infection. Our aim was to further investigate the roles of serum antibodies and viral extra-intestinal spread in diabetes acceleration by rotavirus. Methods Rotavirus-specific serum antibody production was detected by ELISA in diabetes-prone mice given either inactivated or low-dose RRV, in relation to their diabetes development. Serum anti-rotavirus antibody titres and infectious virus in lymph nodes were measured in mice given RRV or porcine rotavirus CRW-8. In lymph node cells, rotavirus antigen presence and immune activation were determined by flow cytometry, in conjunction with cytokine mRNA levels. Results Acceleration of diabetes by RRV required virus replication, which correlated with antibody presence. CRW-8 induced similar specific total immunoglobulin and IgA titres to those induced by RRV, but did not accelerate diabetes. RRV alone elicited specific serum IgG antibodies with a T helper (Th)1 bias, spread to regional lymph nodes and activated antigen-presenting cells at these sites. RRV increased Th1-specific cytokine expression in pancreatic lymph nodes. Diabetes onset was more rapid in the RRVinfected mice with the greater Th1 bias. Conclusions/interpretation Acceleration of murine diabetes by rotavirus is virus strain-specific and associated with virus spread to regional lymph nodes, activation of antigenpresenting cells at these sites and induction of a Th1-dominated antibody and cytokine response.

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Section: Introductionmentioning

confidence: 99%

Rotavirus acceleration of murine type 1 diabetes is associated with a T helper 1-dependent specific serum antibody response and virus effects in regional lymph nodes

et al. 2012

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“…Inoculation with the mouse strain EDIM and the human strain Wa caused no clinical signs of hepatobiliary injury, and consistent with the lack of injury, we found no detectable infectious virus within the liver. Previous studies have shown that the extraintestinal spread of rotavirus is strain dependent (22,23,32). In those studies, the presence of virus within the liver was used as a marker of spread (22,23).…”

Section: Vol 81 2007mentioning

confidence: 99%

“…Previous studies have shown that the extraintestinal spread of rotavirus is strain dependent (22,23,32). In those studies, the presence of virus within the liver was used as a marker of spread (22,23). The results of the current study expand on these observations showing that not only is the extraintestinal spread of rotavirus strain dependent but the specific targets of inoculation within the liver vary, which in turn, impacts the subsequent development of clinical manifestations of disease and the survival of the injected mouse.…”

Section: Vol 81 2007mentioning

confidence: 99%

Effect of Rotavirus Strain on the Murine Model of Biliary Atresia

Allen¹,

Jafri²,

Donnelly³

et al. 2007

J Virol

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Biliary atresia is a devastating disorder of the newborn in which afflicted infants develop inflammation and fibrosis of the extrahepatic biliary tract, resulting in cirrhosis and end-stage liver disease. Infection with a virus is thought to be a contributing factor in the etiology of biliary atresia. In the murine model of biliary atresia, perinatal exposure to rhesus rotavirus (RRV) results in biliary epithelial cell infection causing bile duct obstruction. The purpose of this study was to determine if tropism for the biliary epithelial cell was unique to RRV. Newborn mice underwent intraperitoneal injection with five strains of rotavirus: RRV (simian), SA11-FM (simian/bovine), SA11-SM (simian), EDIM (murine), and Wa (human). RRV and SA11-FM caused clinical manifestations of bile duct obstruction and high mortality. SA11-SM caused clinical signs of hepatobiliary injury but the mortality was markedly reduced. EDIM and Wa caused no sign of hepatobiliary disease. The systemic and temporal distribution of viral protein and live virus varied according to the injected strain. Immunohistochemistry revealed that RRV and SA11-FM targeted the biliary epithelial cells. In contrast, SA11-SM was found in the liver but in not in the biliary epithelium. These results indicate that strain-specific characteristics dictate tropism for cells of hepatobiliary origin which in turn impact the ability to induce the murine model of biliary atresia.

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“…The presence of RVA in MLNs has so far been reported in experimental animal models (Brown & Offit, 1998;Crawford et al, 2006;Dharakul et al, 1988;Fenaux et al, 2006;Kim et al, 2011;Mossel & Ramig, 2003; Park et al, Genetic analyses showed that all strains for which the genome was detected in MLNs from autopsied calves and healthy adult cattle were classified as G and/or P (possible) genotypes generally prevalent in bovines (Tables 2 and 3). Also, in most of the cattle that had RVA genomes in both MLNs and intestinal contents, the strains in intestinal contents were genetically identical to those in MLNs.…”

Section: Discussionmentioning

confidence: 99%

“…However, there has been an increasing number of reports of infectious RVA and the viral antigen being detected in sera and various organs, such as mesenteric lymph nodes (MLNs), lungs and livers in humans and animals (Blutt et al, 2003;Crawford et al, 2006;Dharakul et al, 1988;Fenaux et al, 2006;Lynch et al, 2003;Mossel & Ramig, 2003). In experimental animal models, RVA has been detected not only in the gastrointestinal tract but also in extra-intestinal organs, indicating that the virus is able to spread systemically from the gastrointestinal tract (Crawford et al, 2006;Fenaux et al, 2006;Kim et al, 2011;Mossel & Ramig, 2003;Park et al, 2013Park et al, , 2014.…”

Section: Introductionmentioning

confidence: 99%

Persistence of the rotavirus A genome in mesenteric lymph nodes of cattle raised on farms

Mitake

Ito

Okadera

et al. 2015

Journal of General Virology

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Previous studies revealed that rotavirus A (RVA) is present in not only the small intestine but also various organs. It was reported that RVA persisted in mesenteric lymph nodes (MLNs) in experimental models. However, there have been no reports focused on RVA in MLNs of animals under natural conditions. In this study, in order to investigate the persistence of the RVA genome in MLNs in cattle under natural conditions, reverse transcription-semi-nested PCR was carried out to detect RVA genomes in the MLNs from 17 calves that had been subjected to autopsy examinations. RVA genomes were detected in MLNs from 10 ( 60 %) of the 17 autopsied calves. MLNs from 170 healthy adult cattle that had been slaughtered were also examined; 15 (,10 %) of the 170 cattle had RVA genomes in their MLNs, indicating that RNA genomes are found frequently in MLNs of cattle under natural conditions. Genetic analyses revealed that RVAs in MLNs were classified as G and/or P genotypes generally prevalent in bovines. Basically, the strains in intestinal contents were genetically identical to those in MLNs from individual cattle, suggesting that bovine RVAs have the ability to spread from the intestine to MLNs. Furthermore, amongst RVA-positive cattle, six of 10 autopsied calves and 12 of 15 healthy adult cattle were negative for the virus in the intestinal contents, indicating that bovine RVA genomes can persist in MLNs after viral clearance in the digestive tract.

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A Lymphatic Mechanism of Rotavirus Extraintestinal Spread in the Neonatal Mouse

Cited by 63 publications

References 25 publications

Rotavirus acceleration of murine type 1 diabetes is associated with a T helper 1-dependent specific serum antibody response and virus effects in regional lymph nodes

Rotavirus acceleration of murine type 1 diabetes is associated with a T helper 1-dependent specific serum antibody response and virus effects in regional lymph nodes

Effect of Rotavirus Strain on the Murine Model of Biliary Atresia

Persistence of the rotavirus A genome in mesenteric lymph nodes of cattle raised on farms

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