| authorizations: |
registration not required
|
| accessURL: |
http://www.iedb.org/reference/1000566 |
| landingPage: |
http://www.iedb.org/assay/1050348 |
| type: |
Literature
|
| publicationVenue: |
Vaccine
|
| dates: |
1995
|
| study type: | b cell assays |
| subject species: | Venezuelan equine encephalitis virus (strain Trinidad donkey) |
| fullName: |
A R Hunt
J T Roehrig
|
| method: |
ELISA
|
| name: |
Localization of a protective epitope on a Venezuelan equine encephalomyelitis (VEE) virus peptide that protects mice from both epizootic and enzootic VEE virus challenge and is immunogenic in horses.
|
| description: |
This peptide was derived from the 25 amino acid VEE E2 glycoprotein peptide, pep01(STEELFKEYKLTRPYMARCIRCAVG), which was previously defined and described by Hunt AR. et al. Virol 1990
179:701-711.
Sera from mice immunized with peptide 1-19 conjugated to carrier KLH [p1-19(KLH)], were tested by ELISA for reactivity to 5 overlapping peptides representing the amino terminal of the E2 peptide. Peptide 1-19(KLH) elicited a strong antipeptide response (homologous and p9-19), as well as to the longer peptide pep01 (p1-25) and to the viruses (VEE TRD/TC-83). A significant response was observed for peptide alone (without KLH), but the response was not improved with conjugation to KLH. While no virus neutralizing activity was detected following immunization with p1-19, the majority of mice (15/16) were protected from a lethal challenge with VEE TRD (Table 2). Immunization with p1-19 without KLH also elicited responses against p3-10, but not p1-9 or p5-15. Strong reactivity was also observed for p9-19, indicating that the carboxyl terminal may be immunodominant. Mice immunized with free p1-19 and then challenged with lethal dose of VEE TRD were protected (5/5 survived, data not shown).
|
| name: |
iedb
|
| homePage: |
http://www.iedb.org |