Rabu, 11 Maret 2015

New research has exhibited how the HIV virus targets memory T-cells or "veterans", which could potentially change how drugs are used to halt the virus.

This latest research, appearing in the October issue of the Journal of Biological Chemistry, is a huge breakthrough for the George Mason University based researchers who believe their findings will impact the entire field.

Helper T-cells protect the body's immune system by arranging forces to fight off infection. The HIV virus seizes control of helper T-cells, causing T-cell numbers to drop, making the body vulnerable to disease.

Although they appear similar, T-cells are not all the same. "Virgin" cells are those that have never encountered infection, while experienced ones are know as memory helper T-cells. The researchers examined why HIV prefers to attack memory helper T-cells and avoid their similar associates, 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."

Unlike virgin helper T-cells, memory T-cells are very mobile and constantly on the go. The researchers believe this momentum entices the HIV virus, making the memory cell more vulnerable.

Inside a moving memory cell, the moving edge looks like a waterfall. The cell's supporting bone, or cytoskeleton, acts like a muscle pushing the cell to roam. The researchers looked at how HIV infects those memory cells by going into the center, to the nucleus. In order to reach the nucleus, the virus has to cross the cytoskeleton, in other words pass over a wall.

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."

An advantage for HIV is that it is able to mutate very fast. Memory cell soldiers do not recognize the HIV virus, rendering our immune system defenseless against it. In addition to this, the virus kills many memory helper cells. The way HIV mutates makes it a tough target for drugs. Successfully tackling the virus may be better reached by focusing on the cell, as opposed to the virus itself.

The researchers decided their new strategy should aim at a cellular target that HIV depends on to exist, and then shutting it down. For example, if the cell was a house and the virus needed electricity to live in the house, researchers could target electricity. The tricky part will be shutting it down without impacting healthy cells along with it.

Wu and his team are now looking towards existing drugs, especially those used to treat cancer. Cancer cells and HIV cells share the love of migration, meaning cancer drugs that slow down cancer migration could potentially be used to treat HIV.

After six years of investigating and changing their experiments to reach this finding, the researchers from George Mason University will continue long hours in the lab in search of more break throughs, knowing that failure is also a part of research. Wu concludes, "It is challenging to find a scientific discovery. There is no precedent."

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