Identification of an Outer Capsid Glycoprotein of Human Rotavirus by Concanavalin A

Svensson, Lennart

doi:10.1099/0022-1317-65-12-2183

Cited by 12 publications

(12 citation statements)

References 21 publications

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“…However, since convalescent sera from children infected with subgroup I or II rotaviruses reacted equally well with VP3, the major part of the polypeptide is probably exposing common antigenic sites. It is interesting to note that neither VP8 nor VP9, two outer capsid polypeptides Mason et al, 1983;Offit et al, 1983a;Svensson, 1984), were immunoprecipitated by any of the sera, although they were efficiently labelled by [asS]methionine and clearly identified in virus-infected cell lysates (Fig. 1).…”

Section: Discussionmentioning

confidence: 94%

Serum Antibody Responses to Individual Viral Polypeptides in Human Rotavirus Infections

Svensson¹,

Sheshberadaran²,

Vene³

et al. 1987

Journal of General Virology

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SUMMARYA radioimmunoprecipitation assay (RIPA) was used to study the serum antibody responses to individual polypeptides that developed after infection with viruses from human rotavirus subgroups I and II. Paired sera from eight children (1 to 8.5 years of age) were used in the study. Although all of the eight acute sera were negative by the complement fixation test, four of them were positive by RIPA, indicating a previous infection by rotavirus. A significant difference in the number of polypeptides immunoprecipitated was seen among the convalescent sera. The number of polypeptides immunoprecipitated was found to be related to previous infection experience. At most, ten different polypeptides were immunoprecipitated: seven structural polypeptides VPl to VP7 and three non-structural polypeptides, NSl, NS 2 and NS3. No sera immunoprecipitated VP8 or VP9. Acute sera positive by RIPA immunoprecipitated up to five polypeptides, VP1, VP2, VP3, VP4 and VP6. One of the non-structural proteins (NS2) was found to be particularly immunogenic, since antibodies to this polypeptide were detected in several convalescent sera. Among the structural proteins VP2 and VP6 were found to be the two immunodominant polypeptides which were recognized by all convalescent sera. Only three convalescent sera immunoprecipitated VP7, the major type-specific antigen responsible for inducing neutralizing antibodies. Three of four originally seronegative children with no reactivity in the convalescent sera to VP7 developed neutralizing antibodies to a single serotype. One child developed antibodies to two serotypes.

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Section: Discussionmentioning

confidence: 94%

Serum Antibody Responses to Individual Viral Polypeptides in Human Rotavirus Infections

Svensson¹,

Sheshberadaran²,

Vene³

et al. 1987

Journal of General Virology

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“…The RRV supernatant contains a mixture of DLP and TLP. The DLP lack the outer-capsid proteins VP4 and VP7 required for infectivity and, thus, they are noninfectious (entryincompetent), while the TLP contain all structural proteins and thus are infectious (entry-competent) (71). The availability of the two purified preparations allowed us to determine if DCs responded differently to infectious and noninfectious virus.…”

Section: Rrv Infection Stimulates DC Activation and Type I Ifn Producmentioning

confidence: 99%

“…The cells were harvested 2 to 3 days postinfection and freeze-thawed three times. The virions were recovered from the cell lysate after treatment with trichlorotrifluoroethane, followed by two successive rounds of high-speed ultracentrifugation in sucrose-CsCl gradient to separate double-layered particles (DLP) and triple-layered particles (TLP) (71). The purity and identity of the purified DLPs and TLPs were analyzed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and by titration of MA104 cells.…”

Section: Cellsmentioning

confidence: 99%

Role of Interferon Regulatory Factor 3 in Type I Interferon Responses in Rotavirus-Infected Dendritic Cells and Fibroblasts

Douagi

McInerney

Hidmark

et al. 2007

J Virol

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The main pathway for the induction of type I interferons (IFN) by viruses is through the recognition of viral RNA by cytosolic receptors and the subsequent activation of interferon regulatory factor 3 (IRF-3), which drives IFN-␣/␤ transcription. In addition to their role in inducing an antiviral state, type I IFN also play a role in modulating adaptive immune responses, in part via their effects on dendritic cells (DCs). Many viruses have evolved mechanisms to interfere with type I IFN induction, and one recently reported strategy for achieving this is by targeting IRF-3 for degradation, as shown for rotavirus nonstructural protein 1 (NSP1). It was therefore of interest to investigate whether rotavirus-exposed DCs would produce type I IFN and/or mature in response to the virus. Our results demonstrate that IRF-3 was rapidly degraded in rotavirus-infected mouse embryonic fibroblasts (MEFs) and type I IFN was not detected in these cultures. In contrast, rotavirus induced type I IFN production in myeloid DCs (mDCs), resulting in their activation. Type I IFN induction in response to rotavirus was reduced in mDCs from IRF-3 ؊/؊ mice, indicating that IRF-3 was important for mediating the response. Exposure of mDCs to UV-treated rotavirus induced significantly higher type I IFN levels, suggesting that rotavirus-encoded functions also antagonized the response in DCs. However, in contrast to MEFs, this action was not sufficient to completely abrogate type I IFN induction, consistent with a role for DCs as sentinels for virus infection.

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“…However, some monoclonal antibodies react with viruses in both subgroups, so VP6 proteins must also share common epitopes. VP7 is the major outer capsid protein which is glycosylated and has an approximate molecular weight of 34,000 to 40,000 (93,106,163,180,183,207,275,335,350). This protein is responsible for the serotype specificity of the virus (10,92,94,95,106,163,180,337), which was initially determined by virus neutralization (166,402,404).…”

Section: Molecular Biology and Classificationmentioning

confidence: 99%

Human viral gastroenteritis

Christensen

1989

Clin Microbiol Rev

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During the last 15 years, several different groups of fastidious viruses that are responsible for a large proportion of acute viral gastroenteritis cases have been discovered by the electron microscopic examination of stool specimens. This disease is one of the most prevalent and serious clinical syndromes seen around the world, especially in children. Rotaviruses, in the family Reoviridae, and fastidious fecal adenoviruses account for much of the viral gastroenteritis in infants and young children, whereas the small caliciviruses and unclassified astroviruses, and possibly enteric coronaviruses, are responsible for significantly fewer cases overall. In addition to electron microscopy, enzyme immunoassays and other rapid antigen detection systems have been developed to detect rotaviruses and fastidious fecal adenoviruses in the stool specimens of both nonhospitalized patients and those hospitalized for dehydration and electrolyte imbalance. Experimental rotavirus vaccines have also been developed, due to the prevalence and seriousness of rotavirus infection. The small, unclassified Norwalk virus and morphologically similar viruses are responsible for large and small outbreaks of acute gastroenteritis in older children, adolescents, and adults. Hospitalization of older patients infected with these viruses is usually not required, and their laboratory diagnoses have been limited primarily to research laboratories.

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Identification of an Outer Capsid Glycoprotein of Human Rotavirus by Concanavalin A

Cited by 12 publications

References 21 publications

Serum Antibody Responses to Individual Viral Polypeptides in Human Rotavirus Infections

Serum Antibody Responses to Individual Viral Polypeptides in Human Rotavirus Infections

Role of Interferon Regulatory Factor 3 in Type I Interferon Responses in Rotavirus-Infected Dendritic Cells and Fibroblasts

Human viral gastroenteritis

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