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DNA prime/protein boost vaccine strategy in neonatal macaques against simian human immunodeficiency virus
Author(s) -
Rasmussen Robert A.,
HofmannLehmann R.,
Montefiori D.C.,
Li P.L.,
Liska V.,
Vlasak J.,
Baba T.W.,
Schmitz J.E.,
Kuroda M.J.,
Robinson H.L.,
McClure H.M.,
Lu S.,
Hu S.L.,
Rizvi T.A.,
Ruprecht R.M.
Publication year - 2002
Publication title -
journal of medical primatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.31
H-Index - 42
eISSN - 1600-0684
pISSN - 0047-2565
DOI - 10.1034/j.1600-0684.2002.1o019.x
Subject(s) - virology , biology , immunogenicity , simian immunodeficiency virus , vaccination , heterologous , virus , dna vaccination , priming (agriculture) , immunology , immune system , simian , immunization , gene , genetics , germination , botany
Newborn macaques were vaccinated against a chimeric simian human immunodeficiency (SHIV) virus, SHIV‐vpu + , by DNA priming and boosting with homologous HIV‐1 gp160. Following SHIV‐vpu + challenge, containment of infection was observed in 4 of 15 animals given DNA priming/protein boost vaccination and in three of four animals given gp160 boosts only. Rechallenge with homologous virus of six animals that contained the first challenge virus resulted in rapid viral clearance or low viral loads. Upon additional rechallenge with heterologous, pathogenic SHIV89.6P, four of these six animals maintained normal CD4 + T‐cell counts with no or limited SHIV89.6P infection. Our data suggest that humoral and cellular immune mechanisms may have contributed to the containment of SHIV89.6P; however, viral interference with SHIV‐vpu + could also have played a role. Our results indicate that immunogenicity and efficacy of candidate AIDS vaccines are not affected when vaccination is initiated during infancy as compared with later in life.