Table 1.

Compound	Effects on cells and roles in HIV latency	IC50	Ref
IL-2	- Mitogen of T CD4+ lymphocytes - Reduction of the latent pool in patients, but unable to eradicate HIV	106 units per day for 5 days	[49, 50]
IL-7	- Involved in memory T-cells homeostasis - More potent than IL-2 to activate HIV replication from resting cells - Activates different HIV isolates compared with IL-2	10 to 20 ng/ml (R&D)	[53]
Prostratin	- Activates NF-κB via the PKC pathway - Inhibits HIV replication in productively infected cells - Activates cells without induction of proliferation - Minimal side effects on primary cells ex-vivo	0.1 μM	[54–57]
HMBA	- Involved in differentiation of erythroleukemia cells - Activates HIV replication in chronically infected cell lines - Removes nucleosome 1	1 mM	[46]
EMBA	- Compound related to HMBA, with a lower IC50 - Not tested for its role in HIV latency	100 μM	[67]
SAHA	- Compound related to HMBA also known to be an HDAC inhibitor - Tested clinically for cancer therapy - Not tested for its role in HIV latency	1 μM	[68]
Valproic Acid	- Activates HIV replication in latently infected cell lines - Decreases the pool of latently infected cells in human patients undergoing HAART by a mean of 70%	500 mg x2 daily in patients	[43]
Tat	- Main transcriptional activator of the HIV genome - Pleiotropic effects, may activate many pathways and induce TNF-α production - Intrisic propensity to penetrate any cell - A secreted form of the Tat protein localizes in all tissues of transgenic mice at a concentration sufficient to activate HIV replication in vitro	1 μg/ml of recombinant Tat protein exogenously	[59–61]