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Expression and immunogenicity in rats of recombinant adenovirus 5 DNA plasmids and vaccinia virus containing the HTLV‐I‐env gene
Author(s) -
Kazanji Mirdad,
Bomford Robert,
Bessereau JeanLouis,
Schulz Thomas,
de Thé Guy
Publication year - 1997
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/(sici)1097-0215(19970410)71:2<300::aid-ijc27>3.0.co;2-j
Subject(s) - virology , immunogenicity , vaccinia , recombinant dna , orthopoxvirus , virus , biology , plasmid , poxviridae , gene , dna vaccination , recombinant virus , dna , antibody , immunology , genetics
The complete human T‐cell leukemia virus type I (HTLV‐I) env gene was inserted into an expression cassette containing the adenovirus 5 major late promoter (Ad5‐MLP). Recombinant Ad5‐HTLV‐I‐env was obtained by homologous recombination in 293 cells simultaneously transfected by the expression cassette and the genomic DNA of Ad5. In vitro expression of the HTLV‐I‐env gene in the recombinant vector was detected by immunofluorescence and Western blotting. Functional expression of HTLV‐I‐env was confirmed by syncitium formation specifically in HeLa cells infected with Ad5‐HTLV‐I‐env. Two immunization regimens against HTLV‐I were tested in WKY and Fischer F‐344 rats. The first involved WKY rats primed with Ad5‐HTLV‐I‐env or naked DNA plasmids containing the HTLV‐I‐env gene and boosted with Ad5 containing the HTLV‐I‐env gp46 gene or with baculovirusderived recombinant gp46. No antibody against HTLV‐I was detected, while HTLV‐I‐specific cytotoxic T lymphocytes were recovered from all immunized groups but not from controls. The second approach involved Fischer F‐344 rats primed and boosted with recombinant vaccinia virus containing the HTLV‐I‐env gene. Such rats developed antibodies against the HTLV‐I env gp21 and gp46 (non‐neutralizing). After challenge with human HTLV‐I‐producing cells (MT‐2), both immunization regimens were found to induce partial protection. Int. J. Cancer 71:300–307, 1997. © 1997 Wiley‐Liss, Inc.

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