HIV-1 Tat B-cell epitope vaccination was ineffectual in preventing viral rebound after ART cessation: HIV rebound with current ART appears to be due to infection with new endogenous founder virus and not to resurgence of pre-existing Tat-dependent viremia.

CD4 T cell activation, essential for productive HIV infection, is provided initially in acute HIV infection by innate immune system secretion of activating cytokines. This cytokine response wanes with time and long-term activation of CD4 cells is maintained by HIV Tat protein secreted by HIV infected cells. Structured treatment interruption (STI) in well-controlled antiretroviral-treated (ART) subjects was explored a decade ago with a consensus finding that, in most subjects, HIV levels rebounded within four weeks to pre-ART levels.

Exploratory clinical studies of a synthetic HIV-1 Tat epitope vaccine in asymptomatic treatment-naïve and antiretroviral-controlled HIV-1 infected subjects plus healthy uninfected subjects.

TUTI-16 is a synthetic universal HIV-1 Tat epitope vaccine, designed to induce anti-Tat antibodies that block the function of circulating Tat, an HIV encoded protein secreted by HIV-1 infected cells. Circulating Tat activates CD4 T cells, permitting HIV replication and sustained viremia. Safety, immunogenicity and antiretroviral potential of TUTI-16 were explored in a randomized double-blind dose-escalating study in asymptomatic treatment-naïve HIV-1 infected subjects.

A universal anti-HIV-1 Tat epitope vaccine that is fully synthetic and self-adjuvanting.

Circulating HIV-1 Tat protein is essential for maintenance of the chronic HIV replication that predicates both HIV transmission and clinical progression to AIDS/death. A synthetic anti-Tat epitope vaccine (TUTI-16) was designed to induce neutralizing antibodies to Tat and, hopefully, provide immunological control of HIV replication. TUTI-16 is composed of (1) a conserved Tat B cell epitope (Tat 4-12), rendered universal by introducing known variant amino acids at variable positions 7, 9 and 12 during solid phase synthesis, (2) a promiscuous T helper sequence and (3) a lipopeptide toll-like receptor 2 (TLR2) agonist.