Prophylactic vaccines, designed to elicit potent humoral and cellular immune responses to human immunodeficiency virus type 1 (HIV-1) antigens in mucosa, are the important approach to the protection of individuals against HIV-1 infection, since HIV-1 transmission is largely a result of sexual contac
Induction of mucosal IgA following intravaginal administration of inactivated HIV-1-capturing nanospheres in mice
✍ Scribed by Masaki Kawamura; Taichi Naito; Masamichi Ueno; Takami Akagi; Katsuya Hiraishi; Izumi Takai; Masahiko Makino; Takeshi Serizawa; Kazuhisa Sugimura; Mitsuru Akashi; Masanori Baba
- Book ID
- 102380067
- Publisher
- John Wiley and Sons
- Year
- 2002
- Tongue
- English
- Weight
- 300 KB
- Volume
- 66
- Category
- Article
- ISSN
- 0146-6615
- DOI
- 10.1002/jmv.2144
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✦ Synopsis
Abstract
Concanavalin A‐immobilized polystyrene nanospheres (Con A‐NS) were developed for the HIV‐1 vaccine capable of preventing sexual transmission. Con A‐NS could capture efficiently HIV‐1 irrespective of their cell tropism (R5 or X4). Furthermore, Con A‐NS captured equally infectious and heat‐inactivated HIV‐1. Inactivated HIV‐1‐capturing Con A‐NS (HIV‐NS) were intravaginally administered to mice. Heat‐inactivated HIV‐1 alone and Con A‐NS alone were also administered as control immunogens. Vaginal fluids were collected during and after immunization and analyzed for their anti‐HIV‐1 antibody levels. Although the anti‐HIV‐1 IgG antibody was undetectable in any groups, increased anti‐HIV‐1 IgA antibody response was identified in the vaginal fluids of immunized mice with HIV‐NS. The vaginal fluids obtained from the HIV‐NS‐administered mice showed neutralizing activity against the immunizing HIV‐1 strain. A marked difference in vaginal distribution was observed between HIV‐NS and other immunogens, and the toxicity of Con A was reduced by conjugation with nanospheres. Thus, HIV‐NS may have great potential as a prophylactic HIV‐1 vaccine and should be examined further for its efficacy in non‐human primates. J. Med. Virol. 66:291‐298, 2002. © 2002 Wiley‐Liss, Inc.
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