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With >33 million individuals infected with human immunodeficiency virus type 1 (HIV-1) worldwide, and with >2 million more individuals infected every year [1], the need for an effective HIV-1 vaccine has never been greater. With the recent failure of a T cell immunity vaccine to prevent HIV-1 infection, and with the suggestion that the vaccine actually increased the risk of HIV-1 infection in important population subgroups [2], the human immunodeficiency virus (HIV) research community is reexamining the mechanisms mediating both natural protection against HIV-1 in seronegative individuals exposed to HIV-1 and natural viral control among HIV-infected individuals

A critical reassessment of the goals of vaccination is also ongoing. The ideal HIV-1 vaccine should prevent HIV acquisition; however, if this is not possible, reduction in the plasma HIV RNA level “set point” in vaccinated individuals is an important secondary goal. Indeed, HIV-1 transmission is uncommon when the plasma HIV RNA level of the source partner is <2000 copies/mL [3]. Reduction of the viral load set point as a goal of vaccination has spurred interest in a rare group of HIV-infected individuals who naturally control HIV replication in the absence of therapy. These untreated HIV-infected “elite controllers” (ie, patients with plasma HIV RNA levels of <50 copies/mL) and “viremic controllers” (ie, patients with plasma HIV RNA levels of 50–2000 copies/mL) are highly enriched for several host factors associated with T cell–mediated control, including the protective HLA B57 allele [4, 5]; these observations have motivated the development of T cell immunity vaccines for HIV-1. Would decreasing the viral load set point to the levels observed in HIV-infected elite and viremic controllers necessarily prevent clinical progression?

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