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Scientific Priorities

Developed by the DAIDS VAX004 Specimen Access Approval Panel


Genetic and Host Factor Priorities

  1. Are there genetic factors associated with immune responses?
  2. Was randomization adequate, particularly for African Americans (especially with respect to the acquisition endpoint)?
  3. What are the determinants of virus acquisition? (DAIDS is minimally reserving one vial of PBMC/volunteer to host factor analyses, e.g., for use in gene chip studies).
  4. What are the determinants of virus/host equilibrium?

Serology Priorities

  1. Using a refined (e.g., "three-tier") assessment of neutralizing antibodies in volunteers (100 vaccinated, 25 placebo), where should the bar be set for future trials of candidates that induce neutralizing antibodies? This question deserves immediate priority; a small committee of the DAIDS VAX004 Specimen Access Approval Panel will provide input into which isolates should be included.
  2. Are viruses from immunized individuals who became HIV-infected more difficult to neutralize than viruses from those who received placebo and became infected ("sieving")? This question would use a standard panel of neutralizing antibodies from the trial, isolated at the time of initial vaccination (i.e., controls) vs. 6 or 12 or 24 months later, and would have to await the results of #1 above.

Cellular Priorities

  1. Are there any CD4+ T cell responses to measure, especially in vaccinated uninfected individuals? If so,
    • What are the qualitative and quantitative immune responses over time? What is the "bar" to be exceeded in subsequent trials? For example, is there a correlation between CD4+ T cell responses and neutralization responses to MN gp120?
    • Did AIDSVAX "prime" for anamnestic cellular responses to infection? Are high-risk recipients primed for responses to HIV?
  2. Do the full-length sequences of these viruses in placebo infections differ from those in the historical database? This question has broad relevance to HIV vaccine trials.
  3. Did cellular responses result in "sieving"? This question will require longitudinal sequencing, and for example would be useful for identifying changes in envelope epitopes.
  4. What can be learned about cellular responses to HIV during acute infection? Do "higher risk" differ from "lower risk"? Placebo from vaccinated? (These questions should be coordinated with the Acute Infection Network and should, if possible, include data on CD4+ T cell responses.)

Please note: the quality of the processed PBMCs for generating reliable functional data appears to be poor to marginal at best.

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Last Updated April 27, 2007