Functional properties of DENV EDIIIreactive antibodies in human DENV1infected sera and rabbit antiserum to EDIII.
Mol Med Rep
; 14(2): 1799-808, 2016 Aug.
Article
en En
| MEDLINE
| ID: mdl-27357403
ABSTRACT
The envelope domain III (EDIII) of the dengue virus (DENV) has been confirmed to be involved in receptor binding. It is the target of specific neutralizing antibodies, and is considered to be a promising subunit dengue vaccine candidate. However, several recent studies have shown that antiEDIII antibodies contribute little to the neutralizing or enhancing ability of human DENVinfected serum. The present study involved an analysis of the neutralization and antibodydependent enhancement (ADE) activities of EDIIIreactive antibodies in human convalescent sera from patients with primary DENV1 infection and rabbit antiserum immunized with recombinant DENV1 EDIII protein. The results indicated that serum neutralization was not associated with titres of EDIIIbinding antibodies in the human DENV1infected sera. The depletion of antiEDIII antibodies from these serum samples revealed that the antiEDIII antibodies of the patients contributed little to neutralization and ADE. However, the EDIIIreactive antibodies from the rabbit antiserum exhibited protective abilities of neutralization at a high dilution (~150,000) and ADE at a low dilution (~15,000) for the homotypic DENV infection. Notably, the rabbit antiserum displayed ADE activity only at a dilution of 140 for the heterotypic virus infection, which suggests that EDIIIreactive antibodies may be safe in secondary infection with heterotypic viruses. These results suggest that DENV EDIII is not the predominant antigen of the DENV infection process; however, purified or recombinant DENV EDIII may be used as a subunit vaccine to provoke an effective and safe antibody response.
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1
Base de datos:
MEDLINE
Asunto principal:
Proteínas del Envoltorio Viral
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Dengue
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Virus del Dengue
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Dominios Proteicos
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Sueros Inmunes
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Anticuerpos Antivirales
Límite:
Animals
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Humans
Idioma:
En
Revista:
Mol Med Rep
Año:
2016
Tipo del documento:
Article