Latest research shows how cancer drugs can halt HIV virus.

Groundbreaking research may change how drugs are used to halt the HIV virus, as research exhibits how virus targets T-cells.

The October issue of the Journal of Biological Chemistry includes the breakthrough research recently conducted at the George Mason University. Researchers believe this latest research will have an impact on the entire HIV field.

The body’s immune system relies on helper T-cells to arrange forces to fight off infections in the body. The HIV virus grabs control of these helper T-cells, which leads to a drop in their numbers, and puts the body at risk of disease.

While at first glance the T-cells appear similar, they are not the same. The ‘virgin cells’ are the ones that have never been exposed to infection, whereas the memory helper T-cells are the experienced ones. Researchers looked at why HIV likes to attack the memory T-cells rather than the virgin T-cells.

Weifeng Wang, PhD Biosciences ’12, the study’s main author, explains:
“In the body, HIV is able to kill most memory helper cells. We wanted to pursue what makes the difference between memory and naive T-cells on a molecular level.”

The memory T-cells are very mobile and continuously on the go, whereas the virgin T-cells are not. Researchers believe that it is this momentum is enticing to the HIV virus making the memory T-cells vulnerable.

Cytoskeleton Pushes T-Cells to Roam

The moving edge of the moving memory T-cell resembles a waterfall. The cell’s cytoskeleton pushes the cell to roam. Researchers examined how HIV infected those memory T-cells by going into the nucleus. To reach the nucleus the virus must cross the cytoskeleton.

Wu says:
“HIV jumps over the wall by exploiting the cell’s treadmilling process. The HIV virus uses a receptor to attach to the cell for entry. When the virus touches that receptor, it’s like someone ringing the doorbell. That triggers a signal; someone comes out and opens the door. Now the HIV virus can start the treadmill to ‘walk’ along the cytoskeleton towards the center. If the virus goes to naive cells, it cannot do it. Naive cells aren’t sensitive enough. The cytoskeleton of these ‘virgin’ cells is different from the memory cells, and it is not easy for the virus to start the treadmilling process.”

HIV Virus is not Recognized by T-Cells

HIV has the advantage that it is capable of mutating quickly. Memory cells don’t recognize the HIV virus and so the immune system is defenseless against it. In addition, the HIV virus kills off numerous memory helper T-cells. Because of the method the HIV virus mutates it makes it difficult for drugs to target the virus. However, the HIV virus may be better tackled by focusing on cell rather than on the actual virus.

Researchers decided that their new plan of attack should focus on a cellular target that HIV is dependent on and then shutting that cellular target down. The challenge will be to shut down the virus without also having an impact on the healthy stock.

Cancer Drugs May Play a Role

Wu and his team of researchers are looking at drugs that already exist, especially those used in the treatment of cancer. HIV cells and cancer cells both love to migrate, which means those cancer drugs that slow down the migration of cancer have the potential to also be HIV treatments.

At the conclusion of the researchers, six years of investigating the George Mason University team will now change their experiments to reach this finding. They will continue with research in the lab in search of additional breakthroughs.

Wu concludes, “It is challenging to find a scientific discovery. There is no precedent.”


This is exciting news since it has been some time since there has been any significant breakthroughs in the HIV treatment protocol. The idea that new drugs may not be necessary and that existing cancer drugs may become a vital player in the treatment of HIV is promising. Taking this one-step further one might question whether there is any kind of link between HIV and cancer, at least in the manner that it appears that both of these diseases share similar components. As a result, treatments in the future may overlap in a way that we have not previously seen.

1) n.p. (2012, September 27). “Groundbreaking Research Discovers Possible New Way To Fight HIV.” Medical News Today.



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