Journal
JOURNAL OF VIROLOGY
Volume 86, Issue 19, Pages 10533-10539Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.00796-12
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Funding
- Wilhelm Sander Foundation [2004.107.2]
- European Commission [LSHP-CT-2005-018685, LSHP-CT 2006-037611]
- German Research Foundation [TRR60/1]
- H. W. & J. Hector Foundation
- EC FP6/7 Europrise Network of Excellence
- NGIN consortia
- Bill and Melinda Gates GHRC-CAVD Project
- EU Programme EVA Centre for AIDS Reagents, NIBSC, UK (AVIP) [LSHP-CT-2004-503487]
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To explore the efficacy of novel complementary prime-boost immunization regimens in a nonhuman primate model for HIV infection, rhesus monkeys primed by different DNA vaccines were boosted with virus-like particles (VLP) and then challenged by repeated low-dose rectal exposure to simian immunodeficiency virus (SIV). Characteristic of the cellular immune response after the VLP booster immunization were high numbers of SIV-specific, gamma interferon-secreting cells after stimulation with inactivated SIV particles, but not SIV peptides, and the absence of detectable levels of CD8(+) T cell responses. Antibodies specific to SIV Gag and SIV Env could be induced in all animals, but, consistent with a poor neutralizing activity at the time of challenge, vaccinated monkeys were not protected from acquisition of infection and did not control viremia. Surprisingly, vaccinees with high numbers of SIV-specific, gamma interferon-secreting cells were infected fastest during the repeated low-dose exposures and the numbers of these immune cells in vaccinated macaques correlated with susceptibility to infection. Thus, in the absence of protective antibodies or cytotoxic T cell responses, vaccine-induced immune responses may increase the susceptibility to acquisition of immunodeficiency virus infection. The results are consistent with the hypothesis that virus-specific T helper cells mediate this detrimental effect and contribute to the inefficacy of past HIV vaccination attempts (e. g., STEP study).
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