The differential capacity of these E2F factors to promote oncogenic cell growth was associated with their protein stability, and is likely influenced by their normal expression patterns and cooperation with other factors. The development of combination antiretroviral Butylhydroxyanisole therapy for the treatment of HIV infection has produced a marked decline in AIDS and death, but enthusiasm for these treatments in patients with early stages of HIV infection has been tempered by long-term toxicity, such as lipodystrophy and lactic acidosis, dif?culties with maintaining rigorous compliance, and the evolution of drug resistant HIV. The use of these treatments for prolonged periods may not be achievable, and treatment guidelines continue to change. For these reasons, the development of alternate therapies or treatment strategies continues. One such strategy is the administration of intermittent interleukin-2 to augment or preserve immune function. IL-2 is a cytokine that in vivo is 28-demethyl-beta-amyrone secreted by activated T lymphocytes. IL-2 regulates the proliferation, differentiation, and survival of lymphocytes, including CD4 T cells. Increases in CD4 T lymphocyte count arising from the use of intermittent IL-2 in combination with antiretroviral therapy have been demonstrated consistently in a number of randomised clinical trials. The use of recombinant IL-2 has been associated with transient rises of plasma HIV RNA levels in some patients. However, no signi?cant persistent increase in HIV RNA has been observed in IL-2 recipients when compared to controls treated with combination antiretroviral therapy. In fact, a pooled analysis of long-term follow-up data from the ?rst three randomised controlled trials of intermittent IL-2 suggested that IL-2 in combination with antiretroviral therapy produced larger decreases in viral load than antiretroviral therapy alone. One randomised study similarly found that IL-2 in combination with antiretroviral therapy produced larger decreases in viral load than antiretroviral therapy alone, although these findings were not observed in other randomised studies of short duration. Ongoing studies are addressing the clinical consequences of these CD4 T lymphocyte rises and the significance of these findings in terms of current models used to describe the interplay between virus and host in the setting of HIV infection.