Channels • 2022 • Volume 6 • Number 2 Page 13 immunogenic (specifically, which produced the greatest amounts of the currently understood immune correlates of protection against HIV1 infection), while also remaining safe and well-tolerated (Barouch et al., 2018). First, it’s important to briefly explain Barouch et al.’s methods for conducting these two concurrent studies. In order to conduct the APPROACH human trial, Barouch et al. adopted a multicenter, randomized, double-blind, placebo-controlled model. To achieve this model, a relatively wide diversity of participants from different countries/continents was obtained. The researchers recruited a total of 393 participants (ages 18-50) from 12 different, participating clinical locations in Thailand, South Africa, eastern Africa, and the United States. Specifically, 58 participants were from Thailand, 56 from South Africa, 129 from eastern Africa, and 150 from the U.S. This inclusion of participants from different locations around the world, was important due to the fact that the long-term goal of Barouch et al. - as well as many other researchers - is to develop a universal, prophylactic HIV-1 vaccine. Thus, Barouch et al. surely understood that they needed to determine whether or not any differences in safety or immunogenicity between different ethnicities/nationalities existed. Regardless of where the participants came from, however, only healthy/HIV-1-uninfected individuals were recruited for this study. This step worked to further limited study variables - particularly ensuring that any immunogenicity that was measured post- vaccination, was not a result of prior infection with HIV-1. Next, Barouch et al. randomly assigned all the participants into eight different groups (7 test groups and one placebocontrol group). To ensure that one ethnicity/nationality wasn’t entirely in one of these aforementioned groups, the researchers stratified their sample of 393 participants by region, thereby assigning a relatively equal proportion of randomized individuals into one of each of the trial’s eight groups. The seven test (non-placebo) groups were all similar in the fact that they all began with two replication-incompetent Ad26 viral vector priming vaccinations - trivalent Ad26.Mos.HIV vaccine with three different vectors: one expressing 1 Env mosaic antigen and 2 expressing different Gag-Pol mosaic antigens - (given at a dosage of 5x10^10 vp/0.5mL) at week 0 (beginning) and week 12. The groups differed, however, based upon what booster vaccines were given at weeks 24 and 48. Three of the test groups were boosted with the same vaccine used to prime each group (the Ad26 vector vaccine at the same priming dosage), as well as with either a high dose (250µg), low dose (50µg), or absence of Clade C Env gp140 subunit vaccine (with Alum adjuvant). On the other hand, another three groups were boosted at weeks 24 and 48 by an MVA (modified vaccinia ankara) vaccine, as well as with the previously described high dose, low dose, or no dose of the Clade C Env gp140 subunit vaccine in Alum. The MVA vector vaccine was given at a dosage of 10^8 plaque forming units/0.5mL. There was also a 7th test group that was only boosted with the Clade C Env gp140 high dose, in addition to the placebo group that only received 0.9% saline at each vaccination. After administering each vaccination (in which the participants and clinicians weren’t aware which group each participant was in - double-blind), a blood serum sample was subsequently taken from each individual four weeks later (or 6 months after the final vaccination) in order to determine the immune
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