T-20: will long-term use weaken the immune system’s ability to fight HIV?

Paul Blanchard, HIV i-Base

To help successfully control infections by certain microbes, the immune system uses chemical signals – called cytokines – particularly IL-12 (interleukin-12). Researchers have found that the immune systems of people with HIV/AIDS (PHAs) produce significantly less-than-normal amounts of IL-12.

The reduction in production of this vital cytokine may be one factor behind the weakened immunity seen in PHAs. In laboratory experiments, when researchers gave IL-12 to immune cells taken from HIV positive people, these cells were better able to fight microbes, including HIV.

Now researchers at the National Institutes of Health (NIH) in Bethesda, Maryland, have found that in laboratory experiments the experimental anti-HIV drug T-20 suppresses the production of IL-12 by an important group of immune cells called monocytes.

Perhaps these results should not be surprising: T-20, a fusion inhibitor, resembles a small part of the HIV protein called gp41. Proteins from HIV such as gp120, gp41 and p24 have all been found to weaken immune cells in experiments by other researchers. Although the NIH researchers found that T-20 directly affected monocytes, it may also weaken several other types of immune cells.

The NIH researchers note that their findings suggest that studies of T-20 in people should check for the possibility that this drug weakens the immune response. They note that the concentration of T-20 needed to suppress production of IL-12 is similar to that needed to suppress production of HIV in people. Therefore, immune suppression could occur in people taking T- 20.

The immune-suppressive impact of T-20 on people is not likely to be as significant as large doses of the transplant drugs cyclosporin (Neoral, Sandimmune), ProGraf (tacrolimus) or CellCept (mycophenolate mofetil). Nevertheless, it is important that independent scientists continue to investigate the impact of T-20 on the immune system’s ability to fight HIV and other microbes.


  1. Braun MC, Wang JM, Lahey E, et al. Activation of the formyl peptide receptor by the HIV-derived peptide T-20 suppresses interleukin-12 production by human monocytes. Blood 2001;97(11):3531-3536.
  2. Le Y, Jiang S, Hu J, et al. N36, a synthetic Nterminal heptad repeat domain of the HIV1 envelope protein gp41, is an activator of human phagocytes. Clinical Immunology 2000;96(3):23642.
  3. Su SB, Gong WH, Gao JL, et al. T20/DP178, an ectodomain peptide of human immunodeficiency virus type-1 gp41, is an activator of human phagocyte Nformyl peptide receptor. Blood 1999;93(11):388592.
  4. Deng X, Ueda H, Su SB, et al. A synthetic peptide derived from human immunodeficiency virus type 1 gp120 downregulates the expression and function of chemokine receptors CCR5 and CXCR4 in monocytes by activating the 7transmembrane Gproteincoupled receptor FPRL1/LXA4R. Blood 1999;94(4):116573

Source: CATIE-News is written by Sean Hosein with the collaboration of other members of the Canadian AIDS Treatment Information Exchange, in Toronto. Your comments are welcome. Permission to Reproduce: This document is copyrighted by the Canadian AIDS Treatment Information Exchange (CATIE). All CATIE materials may be reprinted and/or distributed without prior permission. However, reprints may not be edited and must include the following text: From Canadian AIDS Treatment Information Exchange (CATIE). For more information visit CATIE’s Information Network at

Links to other websites are current at date of posting but not maintained.