Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0035412 (rhabdomyosarcoma)
 6,156 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Enterovirus 71 (EV71) is the main etiologic agent of hand, foot, and mouth disease (HFMD) and causes frequently severe neurological complications and mortality in young children. The serum neutralizing antibody response is the major indicator of EV71 infection and protective immunity. The current serum neutralization test based on inhibition of cytopathic effect (Nt-CPE) requires manual microscopic examination, which is time-consuming and labor-intensive. In this study, a high-throughput neutralization assay which employs enzyme immunoassay for detecting growth of EV71 in Rhabdomyosarcoma (RD) cells and measuring serum neutralizing antibody (Nt-EIA) against EV71 was developed. RD cells infected with 100 TCID(50) of EV71 for 36-42h had the best performance and were selected for Nt-EIA. One hundred and twenty human sera (59 negative sera, 61 positive sera) were measured for EV71 neutralization antibody titers by Nt-CPE and Nt-EIA. Neutralization antibody titers against EV71 determined by Nt-EIA had a high sensitivity (100%), specificity (94.9%) and agreement (97.5%) by a qualitative comparison with Nt-CPE. In the quantitative comparison, the correlation coefficient between Nt-EIA and Nt-CPE was 0.91 after log transformation. Overall, the Nt-EIA is a suitable alternative assay for the quantitation of EV71 neutralizing antibody to EV71.
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PMID:Development of a high-throughput assay for measuring serum neutralizing antibody against enterovirus 71. 2003 86

The major group human rhinovirus type 8 can enter cells via heparan sulphate. When internalized into ICAM-1 negative rhabdomyosarcoma (RD) cells, HRV8 accumulated in the cells but caused CPE only after 3 days when used at high MOI. Adaptation by three blind passages alternating between RD and HeLa cells resulted in variant HRV8v with decreased stability at acidic pH allowing for productive infection in the absence of ICAM-1. HRV8v produced CPE at 10 times lower MOI within 1 day. Confocal fluorescence microscopy colocalization and the use of pharmacological and dominant negative inhibitors revealed that viral uptake is clathrin, caveolin, and flotillin independent. However, it is blocked by dynasore, amiloride, and EIPA. Furthermore, HRV8v induced FITC-dextran uptake and colocalized with this fluid phase marker. Except for the complete inhibition by dynasore, the entry pathway of HRV8v via HS is similar to that of HRV14 in RD cells that overexpress ICAM-1.
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PMID:Entry of a heparan sulphate-binding HRV8 variant strictly depends on dynamin but not on clathrin, caveolin, and flotillin. 2126 18