Quercetin synergistically reactivates human immunodeficiency virus type 1 latency by activating nuclear factor‑κB.

Highly active antiretroviral therapy (HAART) is very effective in suppressing human immunodeficiency virus type 1 (HIV‑1) replication. However, the treatment is required to be administered for the remainder of an individual's lifetime due to latent HIV‑1 reservoirs. The 'shock‑and‑kill' strategy, which involves using agents to reactivate latent HIV‑1 and subsequently killing latently infected cells in the presence of HAART, was recently proposed. Unfortunately, no agents have currently demonstrated an ability to reactivate latent HIV‑1 in vivo in the absence of toxicity. Therefore, the identification of novel latency activators is required. In order to identify a potential novel agent, the present study investigated the effect of quercetin on latent HIV‑1 reactivation using an established model of HIV‑1 latency. As a marker for reactivation of HIV‑1 in C11 Jurkat cells, the expression of green fluorescent protein, controlled by HIV‑1 long terminal repeat, was observed by fluorescence microscopy. The results of the present study demonstrated that quercetin effectively reactivated latent HIV‑1 gene expression alone, and led to synergistic reactivation when combined with prostratin or valproic acid. In addition, the present study provides evidence that quercetin may reactivate HIV‑1 expression by inducing nuclear factor‑κB nuclear translocation, and that the toxicity of quercetin is lower when compared with various additional activators of HIV‑1. Combined, the results of the present study indicate that quercetin may be an effective agent to disrupt HIV‑1 latency and may be useful in future eradication strategies.