Hypertrophy, Hyperplasia, and Infectious Virus in Gut‐Associated Lymphoid Tissue of Mice after Oral Inoculation with Simian‐Human or Bovine‐Human Reassortant Rotaviruses

Moser, Charlotte A.; Dolfi, Douglas V.; Vietro, Matthew L. Di; Heaton, Penny M.; Offit, Paul A.; Clark, H Fred

doi:10.1086/319294

Cited by 34 publications

(14 citation statements)

References 15 publications

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“…diarrhea of infant mice) and heterologous simian and rhesus (RRV and SA11) RV strains in CD-1 mice. In contrast, neither a simianhuman nor a bovine-human reassortant induced lymphoid hyperplasia in BALB/c mice (20). Therefore, further investigations will be necessary to determine whether the lymphoid hyperplasia induced by RV is dose, strain, or recipient mouse dependent.…”

Section: Discussionmentioning

confidence: 98%

Early Response to Rotavirus Infection Involves Massive B Cell Activation

Blutt¹,

Warfield²,

Lewis

et al. 2002

The Journal of Immunology

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Rotavirus is an acute enteric pathogen which induces severe diarrhea in infants and children. To determine the immune response to rotavirus in vivo, we used a mouse model of rotavirus infection. We observed dramatic increases in the sizes of both Peyer’s patches and mesenteric lymph nodes, but not spleen, between 1 and 6 days after infection with a homologous strain of murine rotavirus, EC wild type. Histological analysis showed large increases in the numbers of lymphocytes in these same tissues in rotavirus-infected mice. Flow cytometric analysis confirmed the increase in numbers of lymphocytes and revealed a large increase in the percentage of activated B, but not T, lymphocytes in both Peyer’s patches and mesenteric lymph nodes of rotavirus-infected mice compared with control mice. Fragment cultures from these tissues established at 3–4 days postinfection contain rotavirus-specific IgM but not IgA Ab. A similar degree of lymphoid hyperplasia and percentage of activated B cells were observed in rotavirus-infected TCR knockout mice. Taken together, our findings show that rotavirus infection, in the context of a normal immune response, induces a large increase in the percentages of activated B cells in the absence of any detectable increase in the percentage of activated T cells, implicating a T cell-independent B cell response as the primary mechanism for initial rotavirus clearance.

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Section: Discussionmentioning

confidence: 98%

Early Response to Rotavirus Infection Involves Massive B Cell Activation

Blutt¹,

Warfield²,

Lewis

et al. 2002

The Journal of Immunology

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“…Additional evidence of the variation in responses in mice to different strains of rotavirus was provided in studies performed by Dr H. Fred Clark and colleagues at the University of Pennsylvania School of Medicine. 11 Virus was detected in mesenteric lymph nodes and Peyer's patches after inoculation of simian-human but not bovine-human reassortants. The implications of these findings for humans, however, are unclear.…”

Section: Intussusception Pathogenesismentioning

confidence: 96%

Intussusception, Rotavirus, and Oral Vaccines: Summary of a Workshop

Peter

Myers²

2002

Pediatrics

140

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ABSTRACT. Rotavirus gastroenteritis continues to cause substantial morbidity and mortality worldwide, despite widespread breastfeeding and use of oral rehydration therapy. This burden of disease indicates that an effective, safe rotavirus vaccine is needed, and in 1998 the first rhesus-human reassortant rotavirus tetravalent vaccine, Rotashield, was licensed in the United States. However, the recommendations for its use were withdrawn in 1999 because of the recognition of an uncommon but serious adverse event, intussusception. A workshop in September 2001 was held to review the subsequent developments and research regarding this association, the proceedings of which are summarized here. Although the pathogenesis of this association remains unknown, epidemiologic evidence supports a causal relationship, with a population attributable risk of ϳ1 per 10 000 (range of 1 in 5000 to 1 in 12 000) vaccine recipients. Whether this association will exist with other candidate rotavirus vaccine strains and whether the attributable risk for intussusception would be similar in other populations administered this vaccine are unclear. Because perceptions of vaccine safety derive from the relative disease burdens of the illness prevented and adverse events induced, the acceptance of rare adverse events may vary substantially in different settings. Nevertheless, a continuing consensus on the need for a safe and effective vaccine to prevent rotavirus gastroenteritis, especially for use in developing countries, exists. Pediatrics 2002;110(6). URL: http://www. pediatrics.org/cgi/content/full/110/6/e67; intussusception, oral vaccines, rotavirus, rotavirus infection, rotavirus vaccines.

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“…Murine rotavirus antigen was detected in the macrophages of Peyer's patches and mesenteric and inguinal lymph nodes of 14-day-old mice at 2 to 7 days postinoculation (2). In a subsequent study, rotavirus was found in Peyer's patches and mesenteric lymph nodes 1 to 10 days after the inoculation of adult mice with the RRV-based Rotashield vaccine preparation (15). Finally, rotavirus strains incompetent for extraintestinal spread following oral inoculation were observed to be unable to spread from a subcutaneous inoculation site, whereas viruses competent for extraintestinal spread were able to spread from the subcutaneous inoculation site (16).…”

mentioning

confidence: 90%

A Lymphatic Mechanism of Rotavirus Extraintestinal Spread in the Neonatal Mouse

Mossel

Ramig

2003

J Virol

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We used the neonatal mouse model of rotavirus infection and virus strains SA11-clone 4 (SA11-Cl4) and Rhesus rotavirus (RRV) to examine the mechanism of the extraintestinal spread of viruses following oral inoculation. The spread-competent viruses, RRV and reassortant R7, demonstrated a temporal progression from the intestine, to the terminal ileum, to the mesenteric lymph nodes (MLN), and to the peripheral tissues. SA11-Cl4 was not found outside the intestine. Reassortant virus S7, which was unable to reach the liver in previous studies (E. C. Mossel and R. F. Ramig, J. Virol. 76:6502-6509, 2002), was recovered from 60% of the MLN, suggesting that there are multiple determinants for the spread of virus from the intestine to the MLN. Phenotypic segregation analysis identified RRV genome segment 6 (VP6) as a secondary determinant of the spread of virus to the MLN (P ‫؍‬ 0.02) in reassortant viruses containing segment 7 from the spreadincompetent parent. These data suggest that in the orally infected neonatal mouse, the extraintestinal spread of rotavirus occurs via a lymphatic pathway, and the spread phenotype is primarily determined by NSP3 and can be modified by VP6.

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Hypertrophy, Hyperplasia, and Infectious Virus in Gut‐Associated Lymphoid Tissue of Mice after Oral Inoculation with Simian‐Human or Bovine‐Human Reassortant Rotaviruses

Cited by 34 publications

References 15 publications

Early Response to Rotavirus Infection Involves Massive B Cell Activation

Early Response to Rotavirus Infection Involves Massive B Cell Activation

Intussusception, Rotavirus, and Oral Vaccines: Summary of a Workshop

A Lymphatic Mechanism of Rotavirus Extraintestinal Spread in the Neonatal Mouse

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